Resveratrol drives cancer cell senescence via enhancing p38MAPK and DLC1 expressions

Yan Bian1, Xingjie Wang1, Zhaodi Zheng1

  • 1Shandong Provincial Key Laboratory of Animal Resistant Biology, School of Life Sciences, Shandong Normal University, Jinan, 250014, Shandong, China. grli@sdnu.edu.cn.

Food & Function
|March 2, 2022
PubMed

Insights

Resveratrol induces cancer cell senescence, a new anti-cancer approach, by activating ER-stress. This research clarifies resveratrol

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • Pro-senescence therapy is an emerging anti-cancer strategy.
  • Resveratrol exhibits potential cancer-preventive and suppressive properties.
  • The precise mechanisms by which resveratrol induces cancer cell senescence remain largely unknown.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying resveratrol-induced cancer cell senescence.
  • To investigate the role of ER-stress in resveratrol's anti-cancer effects.

Main Methods:

  • Assessed resveratrol's effect on senescence markers (SA-β-Gal activity, colony formation) in breast and lung cancer cells.
  • Investigated the involvement of SIRT1, p38MAPK, NO, and DLC1 in resveratrol-induced ER-stress.
  • Examined the downstream consequences of ER-stress, including DNA damage and mitochondrial dysfunction.

Main Results:

  • Resveratrol induced cancer cell senescence, evidenced by increased SA-β-Gal activity and inhibited colony formation.
  • Resveratrol triggered ER-stress by modulating SIRT1/p38MAPK and NO/DLC1 pathways.
  • ER-stress subsequently led to DNA damage and mitochondrial dysfunction, culminating in senescence.

Conclusions:

  • Resveratrol effectively induces cancer cell senescence through ER-stress activation via the SIRT1/p38MAPK and NO/DLC1 pathways.
  • These findings support resveratrol's potential for clinical cancer therapy and preventive use as a food additive.

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