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. 2022 Apr 21;27(9):2665. doi: 10.3390/molecules27092665

Table 1.

The role of resveratrol in numerous cancers through modulating various cell signaling pathways.

Cancers Finding/Outcome of the Study Ref.
Head and neck cancer Resveratrol enhanced the efficiency of cisplatin and irradiation and resultant decrease of cancer progression [68]
Oral cancer Adhesion of cancer cells treated with resveratrol was decreased and invasive abilities of cancer cells treated with resveratrol were decreased [71]
Resveratrol inhibited cancer through induction of apoptosis [73]
Oesophagus cancer Resveratrol inhibited cancer cell growth in a dose-dependent way through prompting cell cycle arrest [75]
Treatment of cancer cells with resveratrol the PRs of Bcl-2 proteins were seemingly reduced [77]
Lung cancer Apoptosis was induced in TRAIL-resistant lung cancer cells with a cotreatment of resveratrol [78]
Resveratrol caused the tumor outcome via decreasing cell proliferation and promoting cell apoptosis [79]
Resveratrol concentration and time dependently reduced cancer cell viability [80]
Resveratrol synergistically increased the tumor effects of erlotinib [81]
Gastric cancer Resveratrol inhibited the interleukin-6 induced cancer cell invasion [82]
Resveratrol inhibited the growth of cancer cells through preventing the Wnt signaling pathway [83]
Resveratrol was able to significantly inhibit the viability of cancer cells [84]
Resveratrol-induced inhibition of cancer SNU-1 cell proliferation [85]
Gall bladder cancer Resveratrol clearly decreased the proliferation in concentration as well as time-dependent manner and resveratrol induced apoptosis of tumor cells [86]
Bile duct cancer IL-6 indeed promoted the cell migration of invasive cancer cells; the resveratrol powerfully neutralized this effect both in cancer cells [87]
Liver cancer Resveratrol played a role in the inhibition of the proliferation and mobility of carcinoma cells via prompting autophagy [88]
Prevention of cancer cell migration, tumor suppressor gene DLC1 Rho GTPase activating protein level was enhanced with resveratrol treatment [56]
Resveratrol importantly controlled tumor growth [89]
Resveratrol established a potential protective effect on cancer cells in a lipid overload state [90]
Pancreas cancer Resveratrol- and apocynin-treated hamsters exhibited important decrease in the incidence of cancer [91]
Resveratrol inhibited the cell proliferative ability in a dose- and time-dependent manner. [92]
Resveratrol treatment induced apoptosis, inhibited tumor growth, and increased the Bax expression [93]
Resveratrol derivative played role in the induction of dose-dependent apoptosis in cancer cell lines [94]
Colon cancer Resveratrol induced cytotoxicity on cancer cells [95]
Resveratrol efficiently inhibited cell proliferation and promoted cell apoptosis [96]
Resveratrol caused inhibition of cell proliferation interrelated with an induction of apoptosis [97]
Cancer cells exposed to resveratrol displayed meaningfully lower cyclooxygenase-2 and prostaglandin receptor expression [98]
PPARγ playe a role in resveratrol-induced apoptosis [99]
Renal cell carcinoma Sitagliptin/resveratrol combination might signify a useful therapeutic modality for improvement of clear cell renal cell carcinoma [100]
Resveratrol suppressed renal cell carcinoma and migration and promoted carcinoma apoptosis [101]
resveratrol suppressed renal cell carcinoma migration, cell proliferation, and invasion [102]
Resveratrol induced S-phase cell-cycle arrest and caused induction of apoptosis [103]
Prostate cancer Resveratrol and its combination with bicalutamide significantly reduced cell viability [104]
Resveratrol was able to downregulate the levels of the endogenously expressed ARV7 and androgen receptor target gene mRNAs in prostate cancer cells [105]
Resveratrol, DTX, and a combined drug treatment upregulated the proapoptotic genes [64]
Bladder cancer Resveratrol was revealed to significantly inhibit the expression and secretion of matrix metalloproteinase-2 [106]
Resveratrol decreased cell proliferation and induced DNA damage [107]
The effect of resveratrol on cancer cell apoptosis was due to miR-21 regulation of the Akt/Bcl-2 signaling pathway [108]
Resveratrol treatment decreased the expression of thevascular endothelial growth factor [109]
Breast cancer Resveratrol-induced chemosensitivity, cell cycle, and apoptosis were arrested [110]
Proanthocyanidins and resveratrol synergistically inhibited breast cancer cells via inducing apoptosis and modulating DNA methylation [111]
Suppression of EZH2 expression through ERK1/2 dephosphorylation was significant for the antiproliferative activities of resveratrol against breast cancer cells [112]
Cell cycle arrest, caspase activation as well apoptotic induction in cells treated with resveratrol-salinomycin combination established the efficiency of the combination [113]
Endometrial cancer Resveratrol treatment inhibited the growth of cancer cells in a dose-dependent manner [114]
Resveratrol arbitrated suppression of a functional activity of progesterone receptor as established by downregulation of alpha one integrin expression [115]
Cervix cancer Resveratrol treatment with various concentrations caused increased cell cycle arrest [116]
Resveratrol showed a role in the inhibition of both NF-κB and AP-1-mediated metalloproteinase-9 expression [117]
Long treatment of resveratrol induced cytosolic translocation of cytochrome c, caspase-3 activation, and apoptotic cell death [118]
Resveratrol pretreatment caused inhibition of cell division and induced an early S-phase cell-cycle checkpoint arrest [119]
Ovarian cancer ARHI was expressed in low levels in ovarian cancer cell lines, which was enhanced after resveratrol treatment accompanied by growth arrest [120]
Resveratrol analogues decreased the expression of epithelial mesenchymal transition markers [121]
Resveratrol induced apoptotic cell death in dose- and time-dependent manners [122]
Uterine cervix Resveratrol inhibited cell proliferation in the cancer cell line, and the number of apoptotic cells increased in a resveratrol dose-dependent manner [123]
Lymphoma Resveratrol suppressed the phosphorylation level of AKT and Stat3 [124]
Resveratrol played a role as proliferative and proapoptotic activity [125]
Resveratrol treatment increased reactive oxygen species generation, and the reactive oxygen species scavenger could decrease both the resveratrol-induced caspase-3 activity and the formation of acidic vacuoles [126]
Resveratrol induced caspase-dependent apoptosis via arresting cell-cycle progression [127]
Resveratrol played a role in the inhibition of protein synthesis, decreasing reactive oxygen species levels [128]
Myeloma NEAT1 overexpression induced proliferation, migration, and invasion of multiple myeloma cells, although resveratrol neutralized its effect [129]
Resveratrol caused proliferative activity in a dose- and time-dependent manner [130]
Resveratrol inhibited proliferation of myeloma cells in a dose- and time-dependent manner [131]
Melanoma Resveratrol treatment inhibited proliferation and promoted melanogenesis of melanoma cells [164]
Treatment of resveratrol in a tumor caused an increase in Cx43 gap junction communication and improved the combination of resveratrol and cisplatin therapeutic effects [132]
Resveratrol may assist as a pioneering therapeutic for melanoma treatment [133]
Resveratrol inhibited cancer cell proliferation and triggered apoptosis [134]
Leukemia Resveratrol inhibited the proliferation as well as induced apoptosis [135]
Resveratroled act as an autophagy modulator and an apoptosis inducer in human leukemia cells [136]
Resveratrol treatment upregulated the expression of PTEN and reduced the expression of p-AKT protein [137]
Osteosarcoma Resveratrol inhibited cancer cell proliferation and tumorigenesis ability [59]
Resveratrol suppressed the cancer cells by preventing the canonical Wnt signaling pathway [138]
Resveratrol inhibited the hypoxia-enhanced proliferation, epithelial to mesenchymal transition process, and the invasion in osteosarcoma [139]
Pro-poptotic effect of resveratrol might be improved by nutrition restriction elicited by l-asparaginase [140]
Thyroid cancer Resveratrol enhanced cell death induced by (131)I on thyroid cancer cell [141]
Resveratrol treatment suppressed thyroid carcinoma cell growth in a dose-dependent manner [142]
Glioblastoma Resveratrol improved glioblastoma-initiating cells to temozolomide-induced apoptosis [143]
Glioma Resveratrol clearly inhibited EMT-induced self-renewal ability of glioma stem cells [144]
Retinoblastoma Resveratrol induced a dose- and time-dependent decrease in tumor cell viability and also caused inhibition of proliferation [145]