TERT attenuated ER stress-induced cell death

Biochem Biophys Res Commun. 2014 May 2;447(2):378-82. doi: 10.1016/j.bbrc.2014.04.034. Epub 2014 Apr 16.

Abstract

Tumor cells are frequently encountered in nutrient-deprived areas, though the mechanisms underlying their survival are unclear. In the present study, we found that depriving cells of glucose caused endoplasmic reticulum stress (ER stress) in a breast cancer cells line, MCF-7, and that specific activation of ER stress increased telomerase reverse transcriptase (TERT) expression. TERT expression would function in counteracting against the stress because over-expression of TERT diminished ER stress-induced cell death. Therefore, the results provide evidence for the underlying mechanisms of tumor progression in stressed conditions, highlighting that ER stress induces TERT expression to withstand environmental stress, a mechanism which we termed the "ER stress-TERT axis".

Keywords: Cancer; Endoplasmic reticulum stress; Telomerase; Telomerase reverse transcriptase.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis*
  • Disease Progression
  • Endoplasmic Reticulum Stress*
  • Glucose / deficiency
  • Humans
  • MCF-7 Cells
  • Neoplasms / enzymology
  • Neoplasms / pathology*
  • Telomerase / physiology*

Substances

  • Telomerase
  • Glucose