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c-Jun N-terminal kinase is required for vitamin E succinate-induced apoptosis in human gastric cancer cells

Kun Wu1, Yan Zhao, Gui-Chang Li

  • 1Department of Nutrition and Food Hygiene, Public Health School, Harbin Medical University, Harbin 150001, Heilongjiang Province, China. wukun@public.hr.hl.cn

World Journal of Gastroenterology
|April 8, 2004
PubMed
Abstract

Insights

Vitamin E succinate (VES) induces apoptosis in gastric cancer cells by activating the c-Jun N-terminal kinase (JNK) pathway. This pathway involves c-Jun, highlighting a potential therapeutic target for gastric cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Gastric cancer remains a significant global health challenge.
  • Identifying novel therapeutic agents and understanding their mechanisms of action are crucial for improving patient outcomes.

Purpose of the Study:

  • To investigate the role of the c-Jun N-terminal kinase (JNK) signaling pathway in vitamin E succinate (VES)-induced apoptosis.
  • To elucidate the molecular mechanisms by which VES triggers cell death in human gastric cancer SGC-7901 cells.

Main Methods:

  • Human gastric cancer SGC-7901 cells were treated with varying concentrations of VES.
  • Apoptosis was assessed using DAPI staining and DNA fragmentation assays.
  • Western blot analysis was employed to measure JNK and phosphorylated JNK (p-JNK) expression.
  • The impact of dominant-negative JNK (DN-JNK) transfection on VES-induced apoptosis and c-Jun expression was evaluated.

Main Results:

  • VES treatment induced significant DNA fragmentation, indicative of apoptosis, in a dose-dependent manner.
  • VES markedly increased the phosphorylation of JNK, with a sustained elevation observed over 24 hours.
  • Transfection with DN-JNK partially blocked VES-induced apoptosis and modulated JNK and c-Jun protein levels.

Conclusions:

  • The JNK signaling pathway plays a critical role in VES-induced apoptosis in human gastric cancer cells.
  • VES-induced apoptosis is mediated through the JNK pathway, involving c-Jun and its downstream targets.
  • These findings suggest that VES and the JNK pathway represent a promising therapeutic strategy for gastric cancer.

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