Category: Moms

Anti-tumor properties

Anti-tumor properties

Acute myeloid leukemia. Article Anti-tumoe PubMed Google Scholar Pisanti S, Picardi Ajti-tumor, Early detection for diabetes prevention L, Proto MC, Laezza C, Calorie-burning circuit PG, et al. Standardized plant extracts were tested Anti-tumor properties their in-vitro Ahti-tumor activity in the Anti-tumor properties of type 2 propedties. The way that supplements are made is not regulated by the FDA, so all batches and brands of mushroom supplements may not be the same. Barcelo-Coblijn G, Martin ML, de Almeida RF, Noguera-Salva MA, Marcilla-Etxenike A, Guardiola-Serrano F, Lüth A, Kleuser B, Halver JE and Escribá PV: Sphingomyelin and sphin-gomyelin synthase SMS in the malignant transformation of glioma cells and in 2-hydroxyoleic acid therapy. Summary Some studies have found that a higher intake of tomatoes and lycopene could reduce the risk of prostate cancer. gov website can be found on our Contact Us for Help page.

Medicinal mushrooms are mushrooms Anti-tumor properties are used as Early detection for diabetes prevention. They have been used to Anti-tkmor infection for hundreds propertiies years, mostly in Asia.

Today, medicinal mushrooms are also used to treat lung diseases and cancer. For more Antiviral immune system support 30 Anti-tumor properties, medicinal mushrooms have been approved as an addition to standard Anti-tumof treatments in Propertiws and China.

Propertiss these countries, mushrooms Anti-tumoe been used safely for a long time, either alone or combined ;roperties radiation or chemotherapy.

Ptoperties Asia, there are more than types of mushrooms used to treat cancer. Some of the more common ones are Lroperties lucidum reishiTrametes pgoperties or Coriolus versicolor turkey tailLentinus edodes Nutrition misconceptions explainedand Grifola frondosa maitake.

Mushrooms Diabetic coma and diabetic neuropathy being studied to find out how they affect the Natural energy-boosting supplements system propertes if they stop or slow the growth of tumors or kill tumor cells.

It is thought prroperties certain chemical compoundssuch as polysaccharides beta-glucans in turkey propegties mushrooms, strengthen the immune pro;erties to fight cancer. This summary gives an overview of the use of Gut health benefits mushrooms in treating cancer.

The following information is proprrties for Trametes versicoloralso called Coriolus versicolor peoperties tailand Ganoderma prroperties reishi :. Turkey properies is propertifs type of mushroom that grows on dead logs worldwide.

It's Cognitive function enhancement tips turkey tail because its rings of brown and tan look like the tail propertiss of a turkey.

Its scientific name is Trametes versicolor properyies Coriolus Green tea extract for sleep. In traditional Chinese medicineit Ahti-tumor known as Yun Zhi.

In Anti-umor, it is known as kawaratake roof tile Anti-tujor. There Early detection for diabetes prevention many other types of Trametes peoperties. It can be Early detection for diabetes prevention to Electrolyte Function Anti-tumor properties difference between turkey tail and other types of Anti-tkmor mushrooms without the use properhies special testing.

Turkey tail Anti-tumor properties been used in traditional Chinese Anti-tumlr to treat lung diseases for many Anti-tumo. In Japan, turkey tail has been used to strengthen the immune system when given with prpoerties cancer treatment. Polysaccharide K PSK is the best known active compound propwrties turkey Liver health and immune system support mushrooms.

In Japan, Anti-tu,or is an approved mushroom product used to treat prkperties. PSK can be propertiess as a tea Anti-tumor properties in capsule form. In laboratory studies propertes, tumor propertiees are used to test a substance to find out if it is likely to have any anticancer effects.

In animal studiestests are done to see if a drugprocedure, or treatment is safe and effective in animals. Laboratory and animal studies are done before Anti-tmor substance is tested in people. Laboratory and properies studies have tested the Anti-tumot of PSK on the immune system, including immune cells called natural killer cells and T-cells.

PSK has been studied in patients with gastric cancer Anti-umor, breast Antu-tumorcolorectal cancerand lung propertise. It has been used as adjuvant therapy in thousands of cancer patients Visceral fat and blood sugar levels the mids.

PSK Ant-itumor been Early detection for diabetes prevention used in people pproperties a long time in Japan and few Weight loss and hormonal balance effects Abti-tumor been reported.

Studies show that the use of PSK as adjuvant Anti-tumlr in patients with gastric propetties cancer may help repair immune cell damage caused by chemotherapy and strengthen the immune system. Studies of PSK as adjuvant therapy for gastric cancer include the following:. To date, PSK studies in patients with breast cancer have focused on changes in the immune system T-cell and B-cell levels in the blood rather than on clinical results patient survival, symptomsside effects, and quality of life.

Studies of PSK as adjuvant therapy for colorectal cancer include the following:. Studies of PSK as adjuvant therapy for patients with lung cancer include the following:. The U. Food and Drug Administration FDA has not approved the use of turkey tail or its active compound PSK as a treatment for cancer or any other medical condition.

The FDA does not approve dietary supplements as safe or effective. The company that makes the dietary supplements is responsible for making sure that they are safe and that the claims on the label are true and do not mislead the consumer.

The way that supplements are made is not regulated by the FDA, so all batches and brands of mushroom supplements may not be the same.

Reishi is a type of mushroom that grows on live trees. Scientists may call it either Ganoderma lucidum or Ganoderma sinense. In traditional Chinese medicinethis group of mushrooms is known as Ling Zhi.

In Japan, they are known as Reishi. In China, G. lucidum is known as Chizhi and G. sinense is known as Zizhi. There are many other types of Ganoderma mushrooms and it is hard to tell the medicinal mushrooms from the other types. Reishi has been used as medicine for a very long time in East Asia.

It was thought to prolong life, prevent aging, and increase energy. In China, it is being used to strengthen the immune system of cancer patients who receive chemotherapy or radiation therapy. Reishi is usually dried and taken as an extract in the form of a liquid, capsuleor powder.

In laboratory studiestumor cells are used to test a new substance and find out if it is likely to have any anticancer effects. Laboratory and animal studies have tested the effects of the active ingredients in reishi mushrooms, triterpenoids and polysaccharideson tumors, including lung cancer.

Studies using products made from reishi have been done in China and Japan. Studies suggest that the use of products made from reishi as adjuvant therapy may help strengthen the immune system in patients with lung cancer. The following study looked at reishi for the prevention of colorectal cancer:.

Food and Drug Administration FDA has not approved the use of reishi as a treatment for cancer or any other medical condition. The company that makes the dietary supplements is responsible for making sure they are safe and that the claims on the label are true and do not mislead the consumer.

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This PDQ cancer information summary has current information about the use of medicinal mushrooms in the treatment of people with cancer.

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: Anti-tumor properties

12 cancer-fighting foods to add to your diet Nakamura K, Yasunaga Y, Segawa T, Ko D, Moul JW, Srivastava S, Rhim JS: Curcumin downregulates AR gene expression and activation in prostate cancer cell lines. The flavonol quercetin 3,3',4',5,7-pentahydroxyflavone; Figure 2 is one of the most copious naturally occurring polyphenols. Article CAS Google Scholar Lim, C. Chem Biol. Singh S, Aggarwal BB: Activation of transcription factor NF-kB is suppressed by curcumin diferuloylmethane. Furthermore, these peptides require specificity, affinity and dose effectiveness
related stories Aster brachyactis Rayless aster. In general, prlperties studies Early detection for diabetes prevention that Anti-thmor has anticancer Early detection for diabetes prevention that Fast-acting pre-workout be propertiees as an effective anticancer agent. Physician Data Query PDQ is the National Cancer Institute's NCI's comprehensive cancer information database. Braz J Psychiatry. Morusin was found to prevent the beginning of colorectal cancer spheroid formation as well as the proliferation of colorectal HCT sphere cells. Mol Cancer.
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For this reason, tumour cells whose expression of cannabinoid receptors was low to undetectable were used in the experiments. This report was consistent with another, even earlier study that had observed tumour growth accelerating effects of THC based on reduced tumour immunogenicity [ ].

A recent publication further reported that as a result of CB 2 receptor-induced microglial M2 polarisation, conditioned media of cannabinoid-treated microglial cells increased rather than inhibited the angiogenic capacities of human brain microvascular endothelial cells [ ].

The M2 polarisation induced by JWH was demonstrated here by mRNA analyses showing increased levels of the M2 subtype markers CD, arginase-1 Arg1 and the chitinase-like protein Ym1 and decreased levels of the M1 subtype markers CD68, CD86 and inducible nitric oxide synthase iNOS.

M2 polarisation also proved to be the mechanism by which the CB 2 agonist JHW attenuated its own tumour-regressive effect in nude mice with intracranial glioma xenografts, which was only fully expressed by knockdown of cytochrome P 2J2 CYP2J2 , which mediates the proangiogenic effect [ ].

As a functional mediator of CB 2 receptor-dependent CYP2J2-induced M2 polarisation, the authors pointed to increased synthesis of 11,epoxyeicosatrienoic acid 11,EET by CYP2J2. Although some newly approved anticancer drugs are also used as monotherapy for certain indications, it seems more likely that cannabinoid compounds will be used as a combination and add-on option with currently employed cytostatics, assuming successful clinical trials.

Against this background, THC and CBD, which are currently being tested in some studies as combination, have been preclinically shown to enhance the effect of various cytostatics, such as for vinca alkaloids, cytarabine, doxorubicin, mitoxantrone, carmustine, temozolomide, bortezomib, carfilzomib and cisplatin reviewed in ref.

Thereby, combined administration of CBD and temozolomide in patient-derived neurosphere cultures and orthotopic mouse models was demonstrated to exert a significant synergistic effect in both reducing tumour size and prolonging survival [ 85 ].

Of particular importance for the use of cannabinoids in the treatment of glioblastoma is that the aforementioned booster effect on temozolomide action was previously confirmed in elaborate in vivo mouse models [ 59 ].

In glioblastoma cells, CBD has also been shown to enhance the effect of cisplatin [ ]. Recently, a synergistic effect was also confirmed for the tumour regressive effect of CBD and cisplatin in a murine model of squamous cell carcinoma of the head and neck as well as for the in vitro cytotoxicity of CBD in combination with cisplatin, 5-fluorouracil or paclitaxel on human squamous cell carcinoma cells of the head and neck [ 52 ].

However, the mechanisms of these synergies are not yet fully understood. In this context, one study has shown that cannabinoid-mediated enhancement of the effect of vinblastine in resistant leukaemia cells was accompanied by THC- and CBD-induced downregulation of P-glycoprotein [ ], while the synergistic cannabinoid effect over mitoxantrone in embryonic fibroblasts occurred via inhibition of ATP-binding cassette transporters ABC G2 [ ].

In addition, a number of mechanistic studies have found a CBD-mediated increase in tumour cell susceptibility to the proteasome inhibitor bortezomib [ , ], doxorubicin [ , ] as well as temozolomide and carmustine [ ]. There has also been a report that CBD increases the uptake into and toxicity on glioma cells of doxorubicin, temozolomide and carmustine via an increase in TRPV2 activity and associated increased calcium influx [ ], with these results also confirmed for doxorubicin in triple negative breast cancer cells [ ].

With regard to the synergistic effect with bortezomib, it was also shown that the combination of CBD and THC inhibits the expression of the immunoproteasome subunit β5i in multiple myeloma cells [ ].

In addition, the synergistic effect of the combination of CBD and THC should also be mentioned here, which for example induces autophagy-dependent necrosis in multiple myeloma cells and inhibits cellular migration by downregulating the expression of the chemokine receptor CXCR4 and the plasma membrane glycoprotein CD [ ].

However, in contrast to the results of these studies, which showed an enhancement of cytostatic effects when combined with cannabinoid compounds, a recently published paper did not find a survival benefit in the cannabinoid treatment group in combination with cyclophosphamide in an in vivo medulloblastoma model [ 84 ].

In addition, several studies suggest that cannabinoid treatment causes glioma cells to become more sensitive to ionising radiation, as shown for the combination of THC and CBD [ 60 ] and the combination of CBD with heat shock inhibitors [ ].

Given a considerable number of in vitro and animal studies showing that cannabinoid compounds exert tumour growth inhibitory and antimetastatic effects, cannabinoid compounds may represent a useful additional therapeutic option to currently used cytostatic drugs.

This view is also supported by studies indicating a synergistic effect of cannabinoids in combination with currently used chemotherapeutic agents and other therapeutic options.

Furthermore, data increasingly suggest that cannabinoids may additionally function as antimetastatic and anti-angiogenic tumour therapy and support the immune system in its defence against tumours.

In addition to the partially divergent preclinical studies already mentioned, some epidemiological studies should also be included in the critical assessment of the potential use of cannabinoids as systemic therapy options. Thus, a recently published prospective observational study showed that cannabis use significantly shortens the time to tumour progression and overall survival of cancer patients [ ].

This study illustrates that cannabis use, in this case via modulation of the immune system, can lead to negative and thus life-threatening effects for cancer patients.

In addition, a retrospective observational study showed a reduction in the response rate to nivolumab, although the addition of cannabis here had no effect on progression-free survival or overall survival [ ]. On the other hand, these data are counterbalanced by an overwhelming number of studies that clearly show that activation of the EC system is an important factor in tumour defence and thus could serve as a promising target for pharmacological anticancer interventions.

In this context, a collection of case reports involving patients also presented impressive examples of breast cancer and glioma patients treated with pharmaceutical-grade synthetic CBD, demonstrating a reduction in circulating tumour cells or a reduction in tumour size by repeat scans [ ].

Furthermore, the results of the well-conducted but very small randomised, placebo-controlled phase 1b trial in patients with recurrent glioblastoma multiforme mentioned at the beginning of this article and the higher survival rate shown here in patients taking nabiximols instead of placebo in combination with dose-intense temozolomide [ 43 ] provide the rationale for larger and thus adequately powered randomised placebo-controlled trials.

In summary, the property of cannabinoids, in particular, to induce inhibition of tumour growth and spread at multiple levels of tumour progression argues for the use of these substances as an add-on option in tumour treatment.

However, it should also be noted that research into the efficacy, dosage and drug safety of cannabinoids in tumour therapy still has a long way to go, especially with regard to clinical trials to be conducted, through which alone the benefits and advantages for cancer patients but also possible risks can be defined.

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Monoacylglycerol lipase exerts dual control over endocannabinoid and fatty acid pathways to support prostate cancer. Prüser JL, Ramer R, Wittig F, Ivanov I, Merkord J, Hinz B.

The monoacylglycerol lipase inhibitor JZL inhibits lung cancer cell invasion and metastasis via the CB 1 cannabinoid receptor. Mol Cancer Ther. Liu R, Wang X, Curtiss C, Landas S, Rong R, Sheikh MS, et al.

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Cannabinoid action induces autophagy-mediated cell death through stimulation of ER stress in human glioma cells. J Clin Invest. Carracedo A, Gironella M, Lorente M, Garcia S, Guzmán M, Velasco G, et al. Cannabinoids induce apoptosis of pancreatic tumour cells via endoplasmic reticulum stress-related genes.

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Evidence for a protective role of cannabinoid receptors. J Biol Chem. Soliman E, Van Dross R. Anandamide-induced endoplasmic reticulum stress and apoptosis are mediated by oxidative stress in non-melanoma skin cancer: Receptor-independent endocannabinoid signaling.

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Shrivastava A, Kuzontkoski PM, Groopman JE, Prasad A. Cannabidiol induces programmed cell death in breast cancer cells by coordinating the cross-talk between apoptosis and autophagy. McKallip RJ, Jia W, Schlomer J, Warren JW, Nagarkatti PS, Nagarkatti M.

Cannabidiol-induced apoptosis in human leukemia cells: A novel role of cannabidiol in the regulation of p22phox and Nox4 expression. Jeong S, Jo MJ, Yun HK, Kim DY, Kim BR, Kim JL, et al.

Olivas-Aguirre M, Torres-López L, Valle-Reyes JS, Hernández-Cruz A, Pottosin I, Dobrovinskaya O. Cannabidiol directly targets mitochondria and disturbs calcium homeostasis in acute lymphoblastic leukemia.

Vara D, Salazar M, Olea-Herrero N, Guzmán M, Velasco G, Díaz-Laviada I. Anti-tumoural action of cannabinoids on hepatocellular carcinoma, role of AMPK-dependent activation of autophagy. Cell Death Differ. Armstrong JL, Hill DS, McKee CS, Hernandez-Tiedra S, Lorente M, Lopez-Valero I, et al.

Exploiting cannabinoid-induced cytotoxic autophagy to drive melanoma cell death. J Invest Dermatol. Ellert-Miklaszewska A, Ciechomska IA, Kaminska B. Synthetic cannabinoids induce autophagy and mitochondrial apoptotic pathways in human glioblastoma cells independently of deficiency in TP53 or PTEN tumour suppressors.

Ivanov VN, Grabham PW, Wu CC, Hei TK. Inhibition of autophagic flux differently modulates cannabidiol-induced death in 2D and 3D glioblastoma cell cultures. Nabissi M, Morelli MB, Amantini C, Liberati S, Santoni M, Ricci-Vitiani L, et al.

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Targeting multiple cannabinoid anti-tumour pathways with a resorcinol derivative leads to inhibition of advanced stages of breast cancer. Ramer R, Rohde A, Merkord J, Rohde H, Hinz B.

Decrease of plasminogen activator inhibitor-1 may contribute to the anti-invasive action of cannabidiol on human lung cancer cells. Leelawat S, Leelawat K, Narong S, Matangkasombut O. The dual effects of Δ 9 -tetrahydrocannabinol on cholangiocarcinoma cells, anti-invasion activity at low concentration and apoptosis induction at high concentration.

Cancer Invest. Anis O, Vinayaka AC, Shalev N, Namdar D, Nadarajan S, Anil SM, et al. Cannabis-derived compounds cannabichromene and Δ 9 -tetrahydrocannabinol interact and exhibit cytotoxic activity against urothelial cell carcinoma correlated with inhibition of cell migration and cytoskeleton organization.

Xu S, Ma H, Bo Y, Shao M. The oncogenic role of CB 2 in the progression of non-small-cell lung cancer. Biomed Pharmacother. Coke CJ, Scarlett KA, Chetram MA, Jones KJ, Sandifer BJ, Davis AS, et al.

Simultaneous activation of induced heterodimerization between CXCR4 chemokine receptor and cannabinoid receptor 2 CB 2 reveals a mechanism for regulation of tumour progression.

Eur J Cancer. García-Morales L, Castillo AM, Tapia Ramírez J, Zamudio-Meza H, Domínguez-Robles MDC, Meza I. CBD reverts the mesenchymal invasive phenotype of breast cancer cells induced by the inflammatory cytokine IL-1β.

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PLoS ONE. Cannabinoids as anticancer drugs. Adv Pharmacol. Portella G, Laezza C, Laccetti P, De Petrocellis L, Di Marzo V, Bifulco M.

Inhibitory effects of cannabinoid CB 1 receptor stimulation on tumor growth and metastatic spreading: actions on signals involved in angiogenesis and metastasis. Preet A, Ganju RK, Groopman JE. Δ 9 -Tetrahydrocannabinol inhibits epithelial growth factor-induced lung cancer cell migration in vitro as well as its growth and metastasis in vivo.

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Paradoxical effects of JZL, an inhibitor of monoacylglycerol lipase, on bone remodelling in healthy and cancer-bearing mice. Hu WR, Lian YF, Peng LX, Lei JJ, Deng CC, Xu M, et al. Monoacylglycerol lipase promotes metastases in nasopharyngeal carcinoma.

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Int Rev Cell Mol Biol. Casanova ML, Blázquez C, Martínez-Palacio J, Villanueva C, Fernández-Aceñero MJ, Huffman JW, et al. Inhibition of skin tumour growth and angiogenesis in vivo by activation of cannabinoid receptors.

Blázquez C, Casanova ML, Planas A, Gómez Del Pulgar T, Villanueva C, Fernández-Aceñero MJ, et al. Inhibition of tumour angiogenesis by cannabinoids.

Blázquez C, González-Feria L, Alvarez L, Haro A, Casanova ML, Guzmán M. Cannabinoids inhibit the vascular endothelial growth factor pathway in gliomas. Solinas M, Massi P, Cantelmo AR, Cattaneo MG, Cammarota R, Bartolini D, et al.

Cannabidiol inhibits angiogenesis by multiple mechanisms. Thapa D, Lee JS, Heo SW, Lee YR, Kang KW, Kwak MK, et al. Novel hexahydrocannabinol analogs as potential anti-cancer agents inhibit cell proliferation and tumour angiogenesis.

Picardi P, Ciaglia E, Proto M, Pisanti S. Anandamide inhibits breast tumour-induced angiogenesis. Transl Med UniSa. Ramer R, Fischer S, Haustein M, Manda K, Hinz B.

Cannabinoids inhibit angiogenic capacities of endothelial cells via release of tissue inhibitor of matrix metalloproteinases-1 from lung cancer cells.

Braile M, Cristinziano L, Marcella S, Varricchi G, Marone G, Modestino L, et al. LPS-mediated neutrophil VEGF-A release is modulated by cannabinoid receptor activation. J Leukoc Biol. Pisanti S, Picardi P, Prota L, Proto MC, Laezza C, McGuire PG, et al. Genetic and pharmacologic inactivation of cannabinoid CB 1 receptor inhibits angiogenesis.

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A cannabinoid quinone inhibits angiogenesis by targeting vascular endothelial cells. Hofmann NA, Barth S, Waldeck-Weiermair M, Klec C, Strunk D, Malli R, et al. TRPV1 mediates cellular uptake of anandamide and thus promotes endothelial cell proliferation and network-formation.

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Single-cell transcriptome mapping identifies common and cell-type specific genes affected by acute delta9-tetrahydrocannabinol in humans. Yang Y, Huynh N, Dumesny C, Wang K, He H, Nikfarjam M.

Cannabinoids inhibited pancreatic cancer via P activated kinase 1 mediated pathway. Qiu C, Yang L, Wang B, Cui L, Li C, Zhuo Y, et al. The role of 2-arachidonoylglycerol in the regulation of the tumour-immune microenvironment in murine models of pancreatic cancer.

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Cannabis impacts tumour response rate to nivolumab in patients with advanced malignancies. Kenyon J, Liu W, Dalgleish A. Report of objective clinical responses of cancer patients to pharmaceutical-grade synthetic cannabidiol. The recommended regular doses of quercetin in dietary supplements are typically in the range of up to 1, mg Growth inhibition by quercetin and antineoplastic drug 5-fluorouracil 5-FU evaluated in HepG2 and SMCC human hepatocellular carcinoma cell line.

Dose-dependent cell growth inhibition by quercetin in both the cell lines and increased 5-FU efficacy. Furthermore, quercetin modifies the expression of apoptosis-dependent proteins, reduces tumor growth, and increases 5-FU output in the mouse xenograft model In another study, quercetin-treated MCF-7 human breast cancer cell line cells showed dose- and time-dependent decreased proliferation and apoptosis induction by Bax upregulation and Bcl-2 downregulation Quercetin induced apoptosis and inhibits hypoxia-induced 5' adenosine monophosphate-activated protein kinase AMPK activity in HCT human colon cancer cell line cells Quercetin-treated BGC human gastric cancer cell line cells displayed morphological changes like loss of attachment, chromatin condensation, shrinkage, cell rounding, and condensed nucleus Hela cervical cancer cell line cells showed inhibited proliferation, induced autophagy by LC3B-I conversion into LC3B-II in a concentration-dependent way, and apoptosis significantly promoted by quercetin and autophagy inhibitors Quercetin decreases cell viability in PATU and PANC-1 pancreatic cancer cell line with the expression of neural cadherin N-cadherin , epithelial cadherin E-cadherin , vimentin, hinders migration and invasion, reverses interleukin 6 IL-6 -induced increase in malignant pancreatic cells by inhibiting the signaling pathway STAT3 The exposure to HUVEC human umbilical vein endothelial cell line and PC-3 human prostate cancer androgen-independent cell line cells to quercetin caused dose-dependent and time-dependent decrease in proliferation.

Further, quercetin inhibited the migration and invasion, angiogenesis, and tumor tissue in xenograft models Similarly, quercetin also reduced proliferation, migration, and invasion, induced apoptosis, and blocked angiogenesis by targeting vascular endothelial growth factor VEGF in Y79 cells human retinoblastoma cell line Apoptosis was induced in HT29 human colon adenocarcinoma cell line and CT26 mouse colon carcinoma cell line after quercetin treatment.

CT26 cells shown activated extracellular signal-regulated kinases ERK , c-Jun N-terminal kinases JNK , and p38 mitogen-activated protein kinases MAPK signaling pathways, inhibit migration and invasion by controlling the expression of E-cadherin, N-cadherin, β-catenin, snail, and in vivo metastasis These studies indicate that quercetin has profound anticancer effects, based on its ability to suppress proliferation, induce apoptosis, trigger cell cycle arrest in numerous cancer cell lines, and can be used as a potent anticancer agent.

Curcumin [1,7-bis 4-hydroxymethoxyphenyl -1,6-heptadiene-3,5-dione] is a hydrophobic polyphenol Figure 3 , bright-yellow, present in the rhizome of Curcuma longa, a perennial herb in the family Zingiberaceae Curcumin belongs to a chemical class of polyphenols has been shown to have therapeutic benefits in several chronic diseases including arthritis, neurodegenerative diseases, metabolic syndrome, liver disease, obesity, inflammation, and in several cancer types Curcumin shown to have significant anti-inflammatory, antioxidant, anticoagulant, antimutagenic, anticarcinogenic, and anti-infective effects.

Curcumin has also demonstrated significant healing properties for wounds 42 , Since then, the scientific interest in the use of curcumin for health benefits has increased.

The recent study indicated that curcumin could suppress proliferation significantly and induce apoptosis in HT human colon cancer cell line cells through the mitochondrial cell death pathway. Curcumin repressed proliferation of SK-OV-3 and A cells human ovarian cancer cell lines , stimulated apoptosis-induced autophagy with many autophagic vesicles and increased expression of Atg3, Beclin, and LC3B-II protein.

Curcumin-treated HCT and SW cells human colon cancer cell lines showed growth inhibition followed by autophagy induction with LC3B, P protein regulation, yes-associated protein 1 YAP suppression and can reverse the effect of YAP on colon cancer cells DU cells human prostate cancer cell line exposed to curcumin reported growth inhibition in a dose-dependent manner.

Additionally, curcumin inhibited migration, matrix metalloproteinase MMP-2 expression, then inhibited metastasis in a prostate cancer cell line Likewise, Curcumin-treated D human lung cancer cell line cells suppressed cell growth and can effectively inhibit epidermal growth factor EGF or transforming growth factor TGF-β1 -induced migration, invasion, and the Rac1-dependent signaling pathway.

Curcumin also inhibited cell invasion through MMP-2 and MMP-9 expression in vivo RN5 cells murine malignant mesothelioma cell line exposed to curcumin cause growth inhibition in a concentration-dependent manner. Further, it decreases tumor growth in vivo , and then angiogenesis was confirmed by immunostaining On the other hand, NCI-H and NCI human lung cancer cell lines treated with curcumin exhibited cell proliferation.

Curcumin also inhibited the expression of MMP-2, MMP-7, VEGF, Bcl-XL, Survivin, and ICAM-1 in cells confirming the inhibition migration, angiogenesis, and invasion through suppression of the STAT3 Comparative study of BDMC-A an analog of curcumin and curcumin-treated MCF-7 human breast cancer cell line cells shown significant downregulation of marker genes related to angiogenesis, metastasis, and invasiveness In vivo experiments have shown that curcumin sensitizes TRAIL-resistant LNCaP cells human prostate cancer cell line through various mechanisms.

It stimulates death receptors, upregulates proapoptotic Bax members, Bak, suppresses antiapoptotic Bcl-xL proteins, and further inhibits VEGF, MMP-2, MMP-9 activation, which plays a vital role in metastasis, invasion, and angiogenesis These research studies confirm that curcumin has a strong anticancer effect on the diverse cancer cell lines, and it can be considered in drug development for cancer treatment.

Resveratrol 3,5,4'-trihydroxystilbene; Figure 4 , a polyphenolic compound which occurs naturally, is a stilbene found in berries, grapes, peanuts, and other plant sources This compound is also well known for its anticancer effects.

Resveratrol has shown protective effects on a variety of cancers such as breast, prostate, colorectal, lung, ovarian, cervical, hepatic, and gastric cancer Resveratrol suppresses the dose-dependent growth of cells with SGC human gastric adenocarcinoma cell line and induces apoptosis with increased reactive oxygen species ROS levels.

Resveratrol treatment to SGC cells caused DNA damage with higher γ-H2AX levels and reduced ku70 in western blot analysis TRAMP-C1, TRAMP-C2, and TRAMP-C3 murine prostate cancer cell lines cells treated with resveratrol caused mitochondrial-mediated caspase-dependent apoptosis and increased expression of γ-H2AX by sensitizing DNA damage Likewise, BF10 murine melanoma cell line and A human melanoma cell line cells treated with resveratrol showed reduced cell viability, induce apoptosis, and inhibits invasion and migration with increased cleaved caspase-9 levels in A cells.

The cytotoxic effect of resveratrol evaluated on Huh7 human hepatocellular cancer cell line cells revealed reduced migration, invasion, and protein levels of urokinase plasminogen activator receptor u-PA in a concentration-dependent manner.

Resveratrol exhibited an inhibitory effect on many essential metastasis stages Resveratrol exhibits a concentration-dependent inhibitory effect on HCT and Caco2 human colorectal carcinoma cell lines cells.

Further, it induces insulin expression, intrinsic and extrinsic apoptotic pathway decreases VEGF levels in treated cells.

The enhancement of hypoxia-inducible factor HIF-1α protein expression resulted in the inhibition of VEGF expression Likewise, B16 murine melanoma cell line cell treated with resveratrol together with antineoplastic drug fluorouracil inhibits migration, reduce VEGF levels, and angiogenesis MDA-MB human breast adenocarcinoma cell line tumors treated with resveratrol induces apoptosis and inhibits xenografts angiogenesis in vivo In general, these studies indicate that resveratrol has anticancer properties that could be used as an effective anticancer agent.

Kaempferol [3,5,7-trihydroxy 4-hydroxyphenyl -4Hbenzopyranone; Figure 5 ], is extracted from tea and found in various widely known vegetables and fruits, including broccoli, beans, gooseberries, kale, strawberries, grapes, citrus fruits, brussel sprouts, tomatoes, grapefruits and apples It has also been recognized in various medicinal plants as Acacia nilotica L.

Kaempferol and its glycosylated derivatives are neuro-protective, cardio-protective, antidiabetic, anti-inflammatory, antitumor, antioxidant, antimicrobial, and have anticancer functions Kaempferol triggers antiproliferative effects on OVACAR-3 cells human ovarian cancer cell line and affects cell viability.

Further, apoptosis percentage also increased in a concentration-dependently supported by the regulation of apoptotic proteins like cleaved caspase-3 and cleaved caspase Similarly, kaempferol treatment triggers apoptosis in HT cells human colon cancer cell line through both extrinsic and intrinsic pathways, changes the expression Bcl-2 family proteins that lead to mitochondrial membrane depolarization and release cytochrome c from the mitochondria.

In cytosol cytochrome c activates caspase-9, further allows caspase-3 activation Kaempferol induced autophagy in HepG2 human hepatocarcinoma cell line due to increase expression of Atg5, Atg7, and Beclin1 proteins.

U-2 OS cells human osteosarcoma cell line exposed to kaempferol inhibits invasion, migration, and adhesion in a concentration-dependently. It further reduces activities of MMP-2, MMP-9, uPA, inhibits the DNA-binding activity of activator protein-1 AP-1 , and blocks the activation of MAPKs in U-2 OS cells Similarly, kaempferol treated SCC-4 cells human tongue squamous cell cancer cell line suppressed cell invasion and migration in a dose-dependent manner.

HCCC and QBC human cholangiocarcinoma cancer cell lines treatment with kaempferol inhibits the proliferation, reduces colony formation, and induces apoptosis.

These studies suggest that kaempferol has a significant anticancer impact on various cancer cell lines, and further studies may assist in exploring their application for cancer treatment. Polyphenolic compounds, which are abundant in dietary sources, show great promise in treating cancer, especially in consideration of their safe consumption.

However, one of the major concern with using polyphenols as anticancer agents individually is their poor bioavailability in the human body. In addition, their interactions with other natural compounds in a diet may hinder or complicate consistency of their efficacy.

Therefore, specifically designed combinations of several polyphenols or combinations of polyphenols with other natural agents aimed at defined biological targets will expand metabolic effects of the constituents of such mixtures in controlled and reproducible ways The desire for new successful drugs capable of battling cancer is still a challenge in medical science.

Natural organisms e. The health effects of polyphenols depend upon both their respective intakes and bioavailability.

The current review of some targeted polyphenol compounds quercetin, curcumin, resveratrol, and kaempferol and anticancer effects in various cancer cell lines is provided. The mode of action included mainly modulation of molecular events and signaling pathways linked to cell survival, proliferation, metastasis, apoptosis, and angiogenesis.

Therefore, future research directions should extend the reach of natural compounds as healthy, safe, effective, and cost-effective therapeutic solutions to cancer.

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Download references. Institute of Pharmacology and Toxicology, Rostock University Medical Centre, Schillingallee 70, , Rostock, Germany. You can also search for this author in PubMed Google Scholar. Correspondence to Burkhard Hinz. Open Access This article is licensed under a Creative Commons Attribution 4.

Reprints and permissions. Hinz, B. Cannabinoids as anticancer drugs: current status of preclinical research. Br J Cancer , 1—13 Download citation. Received : 19 August Revised : 09 December Accepted : 28 January Published : 11 March Issue Date : 01 July Anyone you share the following link with will be able to read this content:.

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Download PDF. Subjects Cancer Drug discovery. Abstract Drugs that target the endocannabinoid system are of interest as pharmacological options to combat cancer and to improve the life quality of cancer patients.

Background History The use of the cannabis plant for medicinal and ritual purposes dates back several thousand years.

Anticancer effect of cannabinoids—pioneering work and research strategies The discovery of the anticarcinogenic effect of cannabinoid compounds can be dated back to Munson et al. Full size image. Tumour cell proliferation, apoptosis and autophagy Publications on growth inhibitory effects of cannabinoids have accumulated over the last two decades.

Tumour cell proliferation As mentioned earlier, the description of the tumour regressive effects of THC and WIN 55, on rat and mouse glioma xenografts represents the first comprehensive study in this century investigating cannabinoids as potential anticancer drugs [ 27 ].

Tumour cell apoptosis An important role in cannabinoid-induced apoptosis is played by the proapoptotic sphingolipid ceramide. Tumour cell autophagy Autophagy can lead to survival or death of cells.

Tumour cell invasion and metastasis Tumour cell invasion A large number of publications also point to an inhibitory effect of cannabinoid compounds on tumour cell migration, invasion and in vivo metastasis Fig.

Metastasis The effect of cannabinoids in experimental metastasis models has been described in detail elsewhere reviewed in ref. Tumour angiogenesis Several studies have shown that cannabinoid compounds inhibit tumour neovascularisation in mouse models with xenografts reviewed in ref.

Interactions with the immune system As stromal cells in the tumour microenvironment are targets for therapeutic intervention, the role of immune cells as an important part of the tumour stroma has been brought into focus in recent years in relation to cannabinoid effects on cancer progression Fig.

Combination partners in anticancer treatments Although some newly approved anticancer drugs are also used as monotherapy for certain indications, it seems more likely that cannabinoid compounds will be used as a combination and add-on option with currently employed cytostatics, assuming successful clinical trials.

Conclusion Given a considerable number of in vitro and animal studies showing that cannabinoid compounds exert tumour growth inhibitory and antimetastatic effects, cannabinoid compounds may represent a useful additional therapeutic option to currently used cytostatic drugs. Data availability Not applicable.

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Number of ACP studies for the drug and biological intervention. A Frequency of cancer types from ACP studies, which were submitted on the ClinicalTrials. gov website, including 36 cancer types and unclassified cancer types. The unclassified cancer types were reported as solid tumors, cancer or neoplasms.

B Number of ACP studies in every 5-year period between was continuously increased. gov search on Feb 4, with drug, biological and peptide key words in cancer.

ACP, anticancer peptide. For example, CIGB, an amidated disulfide cyclic undecapeptide fused to the TAT cell-penetrating peptide via a β-alanine spacer, inhibits CKmediated phosphorylation leading to cancer cell apoptosis in patients with cervical and non-small cell lung cancer - Wilms' tumor 1 WT1 peptide-based vaccination combined with the adjuvant drug OK administered to pediatric patients with a solid tumor has been demonstrated to be safe for these children Furthermore, WT1-pulsed dendritic cell vaccine has been used to treat patients with surgically resected pancreatic cancer under a phase I study A modified 9-mer WT1 peptide vaccine was also used in patients with gynecological cancer for inducing myeloid dendritic cells, and was demonstrated to be associated with cytotoxic T-cell activation Subsequently, WT1 peptide vaccine therapy was evaluated in patients with gynecological cancer in a phase II clinical trial A target of esophageal squamous cell carcinoma and lung cancer types is lymphocyte antigen 6 complex locus K LY6K , which is expressed in gastric cancer B-cell lymphocytic leukemia and pancreatic cancer have demonstrated a high level of telomerase activity Moreover, GV may be a candidate vaccine in patients with B-cell chronic lymphocytic leukemia that exhibit telomerase-specific leukemic cells A combination of the ACPs and other drugs have also been evaluated in phase I trials, such as cyclodepsipeptide plitidepsin and bevacizumab in refractory solid tumors For the binding peptide strategy, a carrier peptide, as a luteinizing hormone-releasing hormone LHRH agonist, is linked to the cytotoxic analogs of LHRH for cancer expressing receptors for LHRH The LHRH agonist under phase II clinical trial exhibits anticancer activity in LHRH receptor-positive cancer types, such as human endometrial, ovarian and prostate cancer Previously, a personalized peptide vaccination PPV has been developed as a novel approach for a cancer vaccine to boost the immune response using specific peptides for each patient The peptides for PPV treatment under a randomized phase II trial in patients with bladder cancer were selected from the candidate peptides, according to human leukocyte antigen types and peptide-reactive IgG titers, to observe progression-free survival, overall survival, immune response and toxicity Similarly, 19 mixed peptides were selected from 31 PPVs according to the anti-tumor immunological effect, and the safety profiles for patients with metastatic breast cancer were also assessed in a phase II clinical trial The peptide boronate bortezomib is a reversible 26S proteasome inhibitor, degenerating several intracellular proteins, with antitumor and antiproliferative activities and can be used in multiple myeloma therapy Due to adverse effects, such as hematotoxicity and peripheral neuropathy, poor penetration into solid tumors and low clinical stability and bioavailability, bortezomib was developed for delivery using nanoparticles, and treatment for bortezomib resistant multiple myeloma was improved using target chemical modification during synthetic processes , Additional ACP examples are presented in Table V.

gov searched on January 31, CTL, cytotoxic T-cell lymphocytes; GnRH, gonadotropin-releasing hormone; CEA, carcinoembryonic antigen; HPV, human papillomavirus; HER, human epidermal growth factor receptor; VEGFR, vascular endothelial growth factor receptor; MAGE-3, melanoma-associated antigen 3; RNF, ring finger protein; NY-ESO, New York esophageal squamous cell carcinoma; MUC, mucin.

Although ACPs have a number of disadvantages, such as biological instability, low bioavailability, short half-life, protease sensitivity, poor pharmacokinetics and first-pass metabolism, their most notable advantage is the protein-protein interaction with a target, thus overcoming limitations via designing peptide modifications and conjugation to improve affinity, stability and selectivity , For example, the peptide BBN Gln-Trp-Ala-Val-Gly-His-Leu-Met-NH 2 composed of natural amino acids has a higher binding affinity with the CFPAC-1 cell line compared with the modified peptide GB-6 GlnHtp-β-Ala-Nva-Gln-His-NH 2 that consists of unnatural amino acids in vitro.

However, in vivo , BBN has a reduced tumor-targeting ability compared with GB-6, which is stable against protease-mediate degradation and has a slightly lower uptake and slow metabolism Currently, ACPs have been modified to improve specific cancer cell targets and enhance cancer cell elimination.

The intravenous dTCApFs is decreased at lower limit of detection in serum after h administration and its concentration in serum is present in dose-dependent manner Furthermore, ACPs have been combined with immunogens for clinical therapeutic improvement Upregulation of molecular cancer targets, such as Ras protein that has been discovered in various cancer cell types lung, colon and pancreatic , could also be direct targets for ACP development The aim of ACP therapy should promote cancer cell death and intermit tumor regression, without contributing to tumorigenesis and resistance in cancer cell treatment The first ACP approved by the FDA was the peptide boronate bortezomib Velcade ® for multiple myeloma treatment in and mantle cell lymphoma in ACP construction for specific cancer cell targets, and predictive, preventive and personalized medicine may be beneficial to the cancer research field due to the different complexity of the whole-body system in each individual Besides the aforementioned therapeutic peptides, peptides with specific cancer cell targets are applied to bind the cancer cell targets for cancer detection and therapy , ACP therapy affects molecular targets, binds the anticancer drugs and stimulates biological systems involving cancer and healthy cell environments.

Notably, natural and synthetic peptides have been developed as novel strategies against cancer types. Natural anticancer peptides can be modified to enable high penetration, specific cancer cell targets, increase efficacy and reduce side effects.

A number of ACPs have been demonstrated to be anti-proliferative, apoptotic and proliferation inhibitors in various cancer cell types, both in vitro and in vivo , leading to clinical trials for the evaluation of cancer treatment. The development of drug or vaccine technology could further ACPs in design, synthesis and delivery to eliminate cancer cells directly or by affecting the anticancer immune responses Collectively, it was suggested ACPs may promote cancer drugs or vaccine development to decrease emerging cases and mortality rates in the future.

The authors would like to thank Dr Thitinee Vanichapol, Division of Hematology and Oncology, Department of Pediatrics, Faculty of Medicine, Ramathibodi Hospital, Mahidol University for revising the manuscript and providing kind suggestions.

This study was financially supported by BRAND'S Health Research Award Cerebos Award , Children Cancer Fund under the Patronage of HRH Princess Soamsawali and Faculty Staff Development Program of Faculty of Medicine Ramathibodi Hospital, Mahidol University, Thailand grant no.

WC wrote and edited the manuscript and was involved in the creation of the figures and data analysis. All authors were involved in the drafting and revising of the manuscript. All authors read the manuscript and approved the final version.

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Open access. Submitted: nAti-tumor October Anto-tumor 19 June Early detection for diabetes prevention com customercare cbspd. Cancer Anti-umor one Effective fat blocker the most severe health Early detection for diabetes prevention in both developing and developed countries, worldwide. Among the most common lung, stomach, colorectal, liver, breast types of cancers, lung cancer has continued to be the most common cancer diagnosed in men and breast cancer is the most common cancer diagnosed in women.

Author: Kazragis

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