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Trichostatin A induces p53-dependent endoplasmic reticulum stress in human colon cancer cells

Limeng Dai1, Gang He1, Kun Zhang2

  • 1Department of Medical Genetics, College of Basic Medical Science, Army Medical University (Third Military Medical University), Chongqing 400038, P.R. China.

Oncology Letters
|January 19, 2019
PubMed

Insights

Trichostatin A (TSA) induces endoplasmic reticulum (ER) stress in colon cancer cells. This anticancer effect is dependent on the p53 protein, influencing cell viability and apoptosis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Trichostatin A (TSA) exhibits anticancer properties, affecting cell cycle, proliferation, and apoptosis.
  • The role of TSA in endoplasmic reticulum (ER) stress and its underlying mechanisms in cancer remain unclear.
  • p53 is known to regulate ER function under stress, but its involvement with TSA-induced ER stress in cancer is poorly understood.

Purpose of the Study:

  • To investigate the mechanism by which TSA induces ER stress in colon cancer cells.
  • To determine the role of p53 in mediating TSA's effects on ER stress and cancer cell fate.

Main Methods:

  • Treatment of wild-type (WT) HCT116 and p53-deficient (TP53(-/-)) HCT116 colon cancer cells with TSA.
  • Analysis of ER stress markers (GRP78, GRP94) and the IRE1α/XBP1 pathway.
  • Luciferase reporter assays to assess XBP1 splicing.
  • Cell viability assays and apoptosis rate measurements.

Main Results:

  • TSA treatment increased ER stress markers GRP78 and GRP94 in WT HCT116 cells.
  • The IRE1α/XBP1 pathway was activated, but XBP1 splicing was reduced in p53-deficient cells.
  • p53 deficiency led to increased cell viability and decreased apoptosis in response to TSA.

Conclusions:

  • TSA induces ER stress in colon cancer cells through a p53-dependent pathway.
  • p53 plays a critical role in mediating TSA's anticancer effects by regulating ER stress responses.
  • These findings offer insights for developing novel cancer therapies targeting the interplay between TSA, ER stress, and p53.
Keywords:
colon cancerendoplasmic reticulum stressp53trichostatin A

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