Resveratrol drives cancer cell senescence <i>via</i> enhancing p38MAPK and DLC1 expressions

Bian, Yan; Xing-jie, Wang; Zheng, Zhaodi; Ren, Guanghui; Qiao, Mengxue; G, Li

doi:10.1039/d1fo02365a

Cited by 13 publications

(13 citation statements)

References 56 publications

(64 reference statements)

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“…14 Our previous results have shown that DLC1 promotes cell senescence through the FoxO3a/NF-κB signaling pathway or endoplasmic reticulum stress after resveratrol treatment in lung and breast cancer cells. 2,22 In the present study, resveratrol enhanced DLC1 expression in MDA-MB-231, MCF-7 and HepG2 cancer cells. Depletion of DLC1 weakened cell senescence and DDR significantly promoted by resveratrol.…”

Section: Discussionsupporting

confidence: 60%

“…19 The results in our laboratory show that the protein levels of DLC1 are significantly increased in a variety of cancer cells treated with resveratrol. 2,[20][21][22] We wondered whether resveratrol could induce cancer cell senescence by promoting DLC1 to trigger DNA damage. In the present study, we explored the impact of resveratrol on cancer cell senescence and the underlying mechanism targeting DLC1, the DYRK1A-EGFR axis and DNA damage.…”

Section: Introductionmentioning

confidence: 99%

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Resveratrol induces DNA damage-mediated cancer cell senescence through the DLC1–DYRK1A–EGFR axis

Liu

et al. 2023

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Section: Discussionsupporting

confidence: 60%

Section: Introductionmentioning

confidence: 99%

Resveratrol induces DNA damage-mediated cancer cell senescence through the DLC1–DYRK1A–EGFR axis

Liu

et al. 2023

Food Funct.

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“…In the present study, we examined cell fate decisions in the RES-treated A549 and H1299 lung cancer cell lines. Consistent with previous findings (Bian et al, 2022;Jiang et al, 2022;, RES reduced lung cancer cell viability, inhibited cell proliferation, and promoted cell senescence and apoptosis. Our results further showed that RES-induced ROS production by inhibiting Nrf2 expression in a dose-and time-dependent manner.…”

Section: Discussionsupporting

confidence: 92%

“…In our study, we first evaluated the activity of RES against A549 and H1299 cells, which are the most commonly used cell lines in antilung cancer studies (Bian et al, 2022; Fan et al, 2020; J. Li et al, 2022; Y. H. Lin, Zhu, et al, 2021; Maj et al, 2021). Consistent with previous studies (Y. H. Lin, Zhu, et al, 2021), we also demonstrated that RES inhibited the growth and induced apoptosis of NSCLC cells.…”

Section: Discussionmentioning

confidence: 99%

“…Given that RES induces a senescence-like phenotype that acts as a tumor-suppressor mechanism (Bian et al, 2022;Chen et al, 2019), we further clarified the relationship between the anticancer effects of RES on lung cancer cells and cell senescence. SA-β-Gal staining was used to assess the cellular senescence state (Figure 2a).…”

Section: Res-induced Cellular Senescence Of Lung Cancer Cells Arreste...mentioning

confidence: 99%

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Destruction of the cellular antioxidant pool contributes to resveratrol‐induced senescence and apoptosis in lung cancer

Liang

Zhou

et al. 2023

Phytotherapy Research

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Resveratrol (RES) has various pharmacological bioactivities and its anticancer effects in lung cancer have been proven. However, the underlying mechanisms of action of RES in lung cancer remain unclear. This study focused on Nrf2-mediated antioxidant systems in RES-treated lung cancer cells. A549 and H1299 cells were treated with various concentrations of RES at different times. RES decreased cell viability, inhibited cell proliferation, and increased the number of senescent and apoptotic cells in a concentration-and time-dependent manner. Moreover, RES-induced lung cancer cell arrest at the G1 phase was accompanied by changes in apoptotic proteins (Bax, Bcl-2, and cleaved caspase 3). Furthermore, RES induced a senescent phenotype along with changes in senescence-related markers (senescence-associated β-galactosidase activity, p21, and p-γH2AX). More importantly, with prolonged exposure time and increased exposure concentration, intracellular reactive oxygen species (ROS) continuously accumulated, resulting in a decrease in Nrf2 and its downstream antioxidant response elements, including CAT, HO-1, NQO1, and SOD1. Meanwhile, RES-induced ROS accumulation and cell apoptosis were reversed by N-acetyl-Lcysteine treatment. Taken together, these results suggest that RES disturb lung cancer cellular homeostasis by destroying the intracellular antioxidant pool to increase ROS production. Our findings provide a new perspective on RES intervention in lung cancer.

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Phytochemical‐mediated modulation of autophagy and endoplasmic reticulum stress as a cancer therapeutic approach

Al Azzani,

Nizami,

Magramane

et al. 2024

Phytotherapy Research

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Autophagy and endoplasmic reticulum (ER) stress are conserved processes that generally promote survival, but can induce cell death when physiological thresholds are crossed. The pro‐survival aspects of these processes are exploited by cancer cells for tumor development and progression. Therefore, anticancer drugs targeting autophagy or ER stress to induce cell death and/or block the pro‐survival aspects are being investigated extensively. Consistently, several phytochemicals have been reported to exert their anticancer effects by modulating autophagy and/or ER stress. Various phytochemicals (e.g., celastrol, curcumin, emodin, resveratrol, among others) activate the unfolded protein response to induce ER stress‐mediated apoptosis through different pathways. Similarly, various phytochemicals induce autophagy through different mechanisms (namely mechanistic target of Rapamycin [mTOR] inhibition). However, phytochemical‐induced autophagy can function either as a cytoprotective mechanism or as programmed cell death type II. Interestingly, at times, the same phytochemical (e.g., 6‐gingerol, emodin, shikonin, among others) can induce cytoprotective autophagy or programmed cell death type II depending on cellular contexts, such as cancer type. Although there is well‐documented mechanistic interplay between autophagy and ER stress, only a one‐way modulation was noted with some phytochemicals (carnosol, capsaicin, cryptotanshinone, guangsangon E, kaempferol, and δ‐tocotrienol): ER stress‐dependent autophagy. Plant extracts are sources of potent phytochemicals and while numerous phytochemicals have been investigated in preclinical and clinical studies, the search for novel phytochemicals with anticancer effects is ongoing from plant extracts used in traditional medicine (e.g., Origanum majorana). Nonetheless, the clinical translation of phytochemicals, a promising avenue for cancer therapeutics, is hindered by several limitations that need to be addressed in future studies.

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Resveratrol drives cancer cell senescence via enhancing p38MAPK and DLC1 expressions

Abstract: Pro-senescence therapy is a recently proposed anti-cancer strategy and has been shown to effectively inhibit cancer. Resveratrol is gaining attention for its cancer preventive and suppressive properties. The mechanisms of...

Cited by 13 publications

References 56 publications

Resveratrol induces DNA damage-mediated cancer cell senescence through the DLC1–DYRK1A–EGFR axis

Resveratrol induces DNA damage-mediated cancer cell senescence through the DLC1–DYRK1A–EGFR axis

Destruction of the cellular antioxidant pool contributes to resveratrol‐induced senescence and apoptosis in lung cancer

Phytochemical‐mediated modulation of autophagy and endoplasmic reticulum stress as a cancer therapeutic approach

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