Apoptosis in colorectal cancer

J Med Life. 2014 Jun 15;7(2):160-4. Epub 2014 Jun 25.

Abstract

Apoptosis is an inborn process that has been preserved during evolution; it allows the cells to systematically inactivate, destroy and dispose of their own components thus leading to their death. This programme can be activated by both intra and extracellular mechanisms. The intracellular components involve a genetically defined development programme while the extracellular aspects regard endogenous proteins, cytokines and hormones as well as xenobiotics, radiations, oxidative stress and hypoxia. The ability of a cell to enter apoptosis as a response to a "death" signal depends on its proliferative status, the position in the cell cycle and also on the controlled expression of those genes that have the capacity of promoting and inhibiting cell death. The fine regulation of these parameters needs to be maintained in order to ensure the physiological environment required for the induction of apoptosis. Any malfunction in any of the steps of controlled cellular death can lead to dysfunctions and, as a consequence, to different pathological conditions. The importance of apoptosis lies in its active nature and in the potential of controlling biological systems.

Keywords: apoptosis; colorectal cancer; colorectal mutagenesis; oncogene bcl-2; tumoral necrosis factor alpha.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis / genetics
  • Apoptosis / physiology*
  • Caenorhabditis elegans
  • Cell Transformation, Neoplastic / pathology*
  • Colorectal Neoplasms / physiopathology*
  • Genes, bcl-2 / genetics*
  • Humans
  • Mutagenesis / genetics
  • Tumor Necrosis Factor-alpha / metabolism*

Substances

  • Tumor Necrosis Factor-alpha