| Properties | Information | |
|---|---|---|
| PhytoCAT-ID | PhytoCAT-225 | |
| Phytochemical name or plant extracts | Resveratrol | |
| PMID | 27498957 | |
| Literature evidence | Collectively, the resveratrol analog HS-1793 might act as a potent radiosensitizer and be a useful adjuvant agent against radiotherapy-resistant hypoxic cells in solid tumors. | |
| IUPAC name | 5-[(E)-2-(4-hydroxyphenyl)ethenyl]benzene-1,3-diol | |
| Phytochemicals’ class or type of plant extracts | Stilbenoid | |
| Source of phytochemicals or plant Extracts | Juniperus polycarpos | |
| Geographical availability | Iran, Lebanon-Syria, North Caucasus, Transcaucasus, Turkey, Turkmenistan | |
| Plant parts | Leaves | |
| Other cancers | Breast cancer, Prostate cancer, Liver cancer, Pancreatic cancer, Stomach cancer | |
| Target gene or protein | PTEN, STAT-3, VDR, BRCA1, EDA, miR-125b-5p, miR-200c-3p, miR-409-3p, miR-122-5p, miR-542-3p, PCNA, Rb, p53, Bcl-2, aromatase, IL-6, p53, HNRNPA1, Caspase 3, MMP9, AURKA, PLK1, PAK1, Bax, CYP19, p21, RAD51, Twist1, EMT , EGF, AHR, ERα, CYP1A1, CYP1B1, GREB1, cAMP | |
| Gene or Protein evidence | RES has also been shown to regulate the STAT3 signaling cascade via its anti-oxidant and anti-inflammatory effects. When MCF-7 cells were stimulated with resveratrol, quercetin or genistein, there was an increase in PTEN protein levels, resveratrol mediated increase in VDR expression would sensitize breast cancer cells to the effects of 1,25-dihydroxyvitamin D(3) and Vitamin D(3) analogs. The dietary supplements N-acetylcysteine and resveratrol inhibit formation of estrogen-DNA adducts in cultured human breast cells and in women, resveratrol regulates apoptotic and cell cycle machinery in breast cancer cells by modulating key tumor-suppressive miRNAs including miR-125b-5p, miR-200c-3p, miR-409-3p, miR-122-5p and miR-542-3p. Little changes in expression of PCNA, Rb, p53, and bcl-2 were observed in the five cell types treated with resveratrol, compared to untreated cells Among various naturally occurring, biologically active compounds, resveratrol and melatonin have been suggested to act as aromatase inhibitors, which make them potential candidates in hormonal treatment of breast cancer. Our results demonstrated that resveratrol significantly reduced cell proliferation and enhanced chemosensitivity in breast cancer cells by inhibiting production of IL-6 and STAT3 activation. Additionally, resveratrol reduces mutant p53 protein aggregation in MDA-MB-231 and HCC-70 cells but not in the wild-type p53 cell line MCF-7. Regulatory role of resveratrol, a microRNA-controlling compound, in HNRNPA1 expression, which is associated with poor prognosis in breast cancer. Here we show that resveratrol arrests cell proliferation, triggers death and decreases the number of colonies of cells that are sensitive to caspase-3-dependent apoptosis (MCF-7 casp-3) and also those that are unresponsive to it (MCF-7vc). After resveratrol treatment, cell adhesion, wound migration, invasion, and MMP-9 activity were significantly decreased in a dose-dependent manner in 4T1 cells (P < 0.05). In summary, we showed for the first time that resveratrol regulates cell cycle progression by targeting AURKA and PLK1. Our results show a significant induction of tumoral Rac activity and a trend in increased expression of the Rac downstream effector PAK1 and other tumor promoting molecules following resveratrol treatment. The present study illustrated that resveratrol impeded the non-genomic induction of estrogen on CYP19. Resveratrol modulates epigenetic regulators of promoter histone methylation and acetylation that restores BRCA1, p53, p21CIP1 in human breast cancer cell lines. Resveratrol (Resv) is a natural compound representing a promising chemosensitizer for cancer treatment that has been shown to sensitize tumor cells through upregulation and phosphorylation of p53 and inhibition of RAD51. However, we discovered that resveratrol, a naturally occurring compound, induced β-TrCP-mediated Twist1 degradation to attenuate MK-2206-induced EMT in breast cancer cells. Resveratrol inhibits the epidermal growth factor-induced epithelial mesenchymal transition in MCF-7 cells In this brief review, we summarize the studies on phytochemicals such as biochanin A, genistein, quercetin, isoliquiritigenin, resveratrol, and grape seed extracts related to their effect on the activation of breast cancer-associated aromatase promoters and discuss their aromatase inhibitory potential to be used as safer chemotherapeutic agents for specific hormone-dependent breast cancer. Kaempferol or resveratrol inhibited dioxin-induced cytochrome P450 1A1 (CYP1A1) and CYP1B1 expression levels and recruitment of AHR, ERα and co-activators to CYP1A1 and CYP1B1. Both phytochemicals induced the expression and recruitment of ERα to gene amplified in breast cancer 1 (GREB1). RNAi-mediated knockdown of ERα in T-47D cells did not affect the inhibitory action of either phytochemical on AHR activity. Resveratrol itself raises intracellular cAMP levels in breast cancer cells in vitro. I | |
| Target pathways | p53-dependent pathway E2/ERalpha/NGB pathway AR and CXCR4 pathway Akt-caspase-9 pathway. STAT3 pathway | |
| IC50 | 17.84 μg/ml against 4T1 | |
| Potency | In conclusion, this study reveals that non-canonical autophagy induced by resveratrol can act as a caspase-independent cell death mechanism in breast cancer cells. | |
| Cell line/ mice model | MCF-7, HeLa, Seg-1, T47D, MDA-MB-231 , HCT116, PC12 , 4T1, ZR-75-1, MDA-MB-435, SKBR-3 | |
| Additional information | Resveratrol reduces mutant p53 protein aggregation in MDA-MB-231 and HCC-70 cells but not in the wild-type p53 cell line MCF-7. The resveratrol analog HS-1793 enhances radiosensitivity of mouse-derived breast cancer cells under hypoxic conditions, Epub 2016 Mar 9. 4-(E)-{(p-tolylimino)-methylbenzene-1,2-diol}, 1 a novel resveratrol analog, differentially regulates estrogen receptors α and β in breast cancer cells. Moreover, resveratrol sensitizes breast cancer cells to respond to UV treatment as a natural bioactive compound. Some dietary phenolics such as resveratrol (RSV), quercetin, isoflavones, epigallocatechin gallate (EGCG), lignans, and curcumin are gaining attention for their chemopreventive properties in preclinical research. Curcumin and resveratrol are two natural compounds with a large body of evidence showing their cytotoxic activity against a wide variety of cancer cells; however, their poor absorption, bioavailability, and low selectivity have limited their clinical use. We report a novel resveratrol-salinomycin combination for targeting ER-positive breast cancer cells and present evidence for successful pre-clinical implementation of resveratrol. It also activates different kinases, such as CK1, CHK2, and AMPK to induce phosphorylation of p53 in S20, suggesting a novel mechanism of p53 activation and chemosensitization to CDDP. | |
| PubChem ID | 445154 | |
| Additional PMIDs | 16061885 17848600 17554206 18164959 19350482 24119558 26459286 27159275 31002359 31004704 31441212 31317586 31141941 31801405 31982837 32342549 33391978 34352281 34216621 32580673 27960279 30346066 12643641 23452621 31817440 11014220 12838319 20846786 29191255 30060527 31185279 31698751 34371789 34252522 11895924 31417252 14563682 17299206 31394671 22785207 27538699 27323060 30142917 33096835 34067547 12710998 15134383 15785317 16611627 18082939 17933449 19747768 19114588 20223651 20631324 24996158 27109433 28605700 30851384 31155753 34010730 34262713 9499448 19219749 28955914 29135943 30042681 30941654 31440879 34502426 10228948 17517524 17059010 16790523 16546976 17513867 21241168 26996623 27498957 30018739 34488773 34859370 11315261 21794976 32326308 28868867 31847250 33851766 12421874 15165403 15047179 15787436 16506809 21992498 23661994 24043896 25862967 28599439 29742465 30421506 32183060 32784973 33946061 34139914 19627089 24433502 27588384 15030235 16118406 24299158 24747163 24978400 31099163 34072744 22481537 18462857 19167446 22583409 23959397 31456191 32012744 21104029 24465597 26423775 34444715 10698352 15735708 17181483 19800779 19056653 22197621 23298290 24905685 25431744 27355345 26890143 26979321 28229117 28396216 17378944 21464939 22977682 26424027 28377996 10402233 18761329 12135100 26276275 18421301 20031172 35163062 30822142 15188005 25242450 24929094 26970359 26759241 28403783 29872500 10571175 32236622 15120416 30822142 | |
| Additional sources of information | https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:262309-1 | |
| Safety | NA |