Relative down-regulation of apoptosis and autophagy genes in colorectal cancer

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06:52

Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres

Published on: July 22, 2020

Ying-Tse Chang1, Hsien-Chun Tseng, Chi-Chou Huang

  • 1Division of Gastroenterology, Tungs' Taichung Metro Harbor Hospital, Taichung County, Taiwan.

European Journal of Clinical Investigation
|October 1, 2010
PubMed
Abstract

Insights

Programmed cell death (PCD) pathways, including apoptosis and autophagy, are disturbed in colorectal cancer. Our study found PCDs are down-regulated in tumor tissues, potentially aiding cancer cell survival.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Death Mechanisms

Background:

  • Colorectal cancer pathogenesis involves dysregulation of programmed cell death (PCD), encompassing apoptosis and autophagy.
  • Investigating these pathways simultaneously is crucial for understanding their pathological roles in colorectal cancer.

Purpose of the Study:

  • To simultaneously investigate apoptosis and autophagy pathways in colorectal cancer.
  • To elucidate the pathological roles of PCDs in colorectal cancer development and progression.

Main Methods:

  • Real-time quantitative PCR (RT-qPCR) array analyzed mRNA levels of 22 apoptosis and autophagy-related genes.
  • 15 paired colorectal tumor and non-cancerous tissue samples were used.
  • Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) served as the reference gene for normalization.

Main Results:

  • GAPDH mRNA levels were significantly higher in tumor tissues (approx. 4.01-fold).
  • After normalization, most analyzed PCD-related genes showed decreased expression in tumor tissues, except for damage-regulated autophagy modulator (DRAM).
  • Gene expression within the same pathway was correlated, with increased correlation for tumor necrosis factor receptor (TNFR) and Akt in tumor tissues.

Conclusions:

  • Elevated GAPDH mRNA may indicate altered metabolic states in cancer cells.
  • Programmed cell death pathways are relatively suppressed in colorectal tumors when considering metabolic state.
  • This suppression of PCD is hypothesized to promote cancer cell survival and tumor progression.

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