DEC2 expression antagonizes cisplatininduced apoptosis in human esophageal squamous cell carcinoma

Hidenobu Sato1, Yunyan Wu1, Yukio Kato2

  • 1Department of Pathology and Bioscience, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori 036‑8562, Japan.

Insights

Differentiated embryonic chondrocyte expressed gene 2 (DEC2) inhibits apoptosis in esophageal cancer cells. Overexpressing DEC2 improves cell viability and reduces cisplatin-induced apoptosis, suggesting therapeutic potential.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • Differentiated embryonic chondrocyte expressed gene 1 (DEC1) and DEC2 are basic helix-loop-helix factors.
  • DEC proteins are implicated in circadian rhythms, hypoxia response, and tumorigenesis.
  • The specific roles of DEC1 and DEC2 in esophageal carcinoma apoptosis are not well understood.

Purpose of the Study:

  • To investigate the roles of DEC1 and DEC2 in the apoptosis of human esophageal squamous cell carcinoma TE-11 cells.
  • To determine the effects of DEC1 and DEC2 expression on apoptosis-related markers and cell viability following cisplatin treatment.

Main Methods:

  • Western blot analysis to assess apoptosis-related marker expression.
  • MTS assay to evaluate overall cell viability.
  • Hematoxylin and eosin staining for apoptosis analysis.

Main Results:

  • Cisplatin treatment downregulated DEC2 and upregulated DEC1 expression.
  • DEC2 overexpression inhibited the pro-apoptotic factor Bim and increased the anti-apoptotic factor Bcl-xL.
  • DEC2 overexpression enhanced cell viability and reduced cisplatin-induced apoptosis, while DEC1 overexpression had no significant effect.

Conclusions:

  • DEC2 exhibits anti-apoptotic effects in TE-11 esophageal squamous cell carcinoma cells.
  • Targeting DEC2 may offer therapeutic potential for esophageal cancer treatment, particularly in combination with cisplatin.