Resveratrol Induces Mitochondrial Apoptosis and Inhibits Epithelial-Mesenchymal Transition in Oral Squamous Cell Carcinoma Cells

Kim, Seong-Eon; Shin, Sang‐Hun; Lee, Jae Yeol; Kim, Chul-Hoon; Chung, Il‐Kwun; Hj, Kang; Park, Hae Ryoun; Park, Bong Soo; Kim, In‐Ryoung

doi:10.1080/01635581.2018.1397708

Cited by 50 publications

(55 citation statements)

References 52 publications

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“… 20 Research by Kim et al showed that res-veratrol induced mitochondrial apoptosis and inhibited cell invasion and migration by inhibiting epithelial–mesenchymal transition in oral squamous cell carcinoma cells. 21 Resvera-trol was also reported to decrease cell viability and proliferation while induced apoptosis in H460 lung cancer cells significantly. 22 Similarly, we also observed that resveratrol suppressed cell proliferation and induced apoptosis in NSCLC cells, indicating the anti-tumor effect of resveratrol in NSCLC progression.…”

Section: Discussionmentioning

confidence: 98%

Resveratrol, an activator of SIRT1, induces protective autophagy in non-small-cell lung cancer via inhibiting Akt/mTOR and activating p38-MAPK

Wang

Cao

et al. 2018

OTT

133

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BackgroundResveratrol, a natural polyphenolic phytoalexin, has potent anti-tumor activity. Recently, it was found to induce autophagy in cancer cells. However, the effects of resveratrol on autophagy in non-small-cell lung cancer (NSCLC) cells have not yet been clearly elucidated.Materials and methodsA549 and H1299 cells were treated with different concentrations of resveratrol. Cell growth and apoptosis were measured by CCK-8 assay and flow cytometry, respectively. A549 cells were then treated with 200 μM resveratrol or SRT1720. Cell autophagy was detected by western blot and immunofluorescence.ResultsIn this study, we found that resveratrol exerted the anti-tumor effect through inhibiting cell proliferation and promoting cell apoptosis in NSCLC cells dose-dependently. Resveratrol has also increased the relative expression of Beclin1 and LC3 II/I while decreased p62 expression, suggesting that resveratrol induced autophagy in NSCLC cells. In addition, resveratrol increased SIRT1 expression and SIRT1 activator SRT1720-induced autophagy of NSCLC cells. SIRT1 knockdown reduced resveratrol-induced autophagy significantly. These results indicated that resveratrol might induce autophagy through upregulating SIRT1 expression. Moreover, inhibiting autophagy by autophagy inhibitor 3-methyladenine or SIRT1 inhibitor nicotinamide significantly suppressed proliferation while promoted apoptosis compared with the resveratrol 200 μM group, suggesting that resveratrol-induced autophagy might act as a protective mechanism to promote NSCLC cell survival and inhibiting autophagy can enhance the anti-tumor effect of resveratrol. Besides that, resveratrol treatment inhibited Akt/mTOR while p38-MAPK was activated in NSCLC cells in a dose-dependent manner. Activating Akt/ mTOR pathway by IGF-1 or inhibiting p-38-MAPK pathway by doramapimod significantly inhibited cell proliferation while increased cell apoptosis of NSCLC cells compared with the resveratrol 200 μM group.ConclusionTaken together, our findings suggest that resveratrol inhibited proliferation but induced apoptosis and autophagy via inhibiting Akt/mTOR and activating p38-MAPK pathway. Resveratrol-induced autophagy might act as a protective mechanism to promote NSCLC cell survival. Therefore, inhibition of autophagy may enhance the anti-tumor activity of resveratrol in NSCLC.

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Section: Discussionmentioning

confidence: 98%

Resveratrol, an activator of SIRT1, induces protective autophagy in non-small-cell lung cancer via inhibiting Akt/mTOR and activating p38-MAPK

Wang

Cao

et al. 2018

OTT

133

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“…In a study by Lei et al (25), RV decreased proliferation, enhanced cellular differentiation and improved melanin generation in HT-144 melanoma cells through inhibiting the mitogen-activated protein kinase kinase/ERK kinase pathway. Kim et al (26) revealed that RV triggered cell death in the mitochondrial pathway. Furthermore, RV reduced survival and enhanced apoptosis in H460 lung cancer cells (27).…”

Section: Discussionmentioning

confidence: 99%

Resveratrol suppresses melanoma growth by promoting autophagy through inhibiting the PI3K/AKT/mTOR signaling pathway

Gong¹,

Xia²

2019

Exp Ther Med

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Resveratrol (RV) is a natural polyphenolic phytoalexin derived from peanuts, red grape skins and red wine, and has been demonstrated to alleviate multiple types of malignancies. However, how RV achieves this in melanoma is unknown. The aim of present study was to investigate the role of RV in melanoma, using Cell Counting Kit-8, flow cytometry and western blot analysis. RV inhibited melanoma cell viability, migration and invasion counteracting melanoma progression. In addition, proteins associated with autophagy, including Beclin 1 and microtubule-associated protein 1A/1B-light chain 3 (LC3)-II/I, were upregulated, whereas p62 expression was downregulated in RV-treated cells. The number of LC3 + puncta, which can be applied to represent autophagosome formation, increased following RV treatment, suggesting that RV may trigger autophagy in melanoma cells. Treatment with the autophagy inhibitor, 3-methyladenine, reversed the RV-dependent inhibition of viability, migration and invasion of melanoma cells. RV treatment also reduced the ratios of phosphorylated (p)-AKT/AKT and p-mTOR/mTOR in melanoma cells. In conclusion, these findings suggested that RV may inhibit the viability and migration of melanoma cells through inhibiting the AKT/mTOR pathway, thus triggering autophagy. This indicated that RV may serve as an innovative therapeutic for melanoma treatment.

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“…In oral squamous cell carcinoma cells, resveratrol can suppress cell invasion and migration by decreasing the expression of EMT-inducing transcription factors. 228 During cancer chemotherapy, acquired Doxorubicin resistance severely impedes the therapeutic effect, invariably leading to poor prognosis. In gastric cancer, resveratrol can reverse Doxorubicin resistance by interfering with the EMT process via modulation of PTEN/Akt signaling.…”

Section: Tcm For Prevention Of Emt and Metastasismentioning

confidence: 99%

Traditional Chinese medicine as a cancer treatment: Modern perspectives of ancient but advanced science

et al. 2019

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Traditional Chinese medicine (TCM) has been practiced for thousands of years and at the present time is widely accepted as an alternative treatment for cancer. In this review, we sought to summarize the molecular and cellular mechanisms underlying the chemopreventive and therapeutic activity of TCM, especially that of the Chinese herbal medicine‐derived phytochemicals curcumin, resveratrol, and berberine. Numerous genes have been reported to be involved when using TCM treatments and so we have selectively highlighted the role of a number of oncogene and tumor suppressor genes in TCM therapy. In addition, the impact of TCM treatment on DNA methylation, histone modification, and the regulation of noncoding RNAs is discussed. Furthermore, we have highlighted studies of TCM therapy that modulate the tumor microenvironment and eliminate cancer stem cells. The information compiled in this review will serve as a solid foundation to formulate hypotheses for future studies on TCM‐based cancer therapy.

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Resveratrol Induces Mitochondrial Apoptosis and Inhibits Epithelial-Mesenchymal Transition in Oral Squamous Cell Carcinoma Cells

Cited by 50 publications

References 52 publications

Resveratrol, an activator of SIRT1, induces protective autophagy in non-small-cell lung cancer via inhibiting Akt/mTOR and activating p38-MAPK

Resveratrol, an activator of SIRT1, induces protective autophagy in non-small-cell lung cancer via inhibiting Akt/mTOR and activating p38-MAPK

Resveratrol suppresses melanoma growth by promoting autophagy through inhibiting the PI3K/AKT/mTOR signaling pathway

Traditional Chinese medicine as a cancer treatment: Modern perspectives of ancient but advanced science

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