UCP2 inhibits ROS-mediated apoptosis in A549 under hypoxic conditions

PLoS One. 2012;7(1):e30714. doi: 10.1371/journal.pone.0030714. Epub 2012 Jan 24.

Abstract

The Crosstalk between a tumor and its hypoxic microenvironment has become increasingly important. However, the exact role of UCP2 function in cancer cells under hypoxia remains unknown. In this study, UCP2 showed anti-apoptotic properties in A549 cells under hypoxic conditions. Over-expression of UCP2 in A549 cells inhibited reactive oxygen species (ROS) accumulation (P<0.001) and apoptosis (P<0.001) compared to the controls when the cells were exposed to hypoxia. Moreover, over-expression of UCP2 inhibited the release of cytochrome C and reduced the activation of caspase-9. Conversely, suppression of UCP2 resulted in the ROS generation (P = 0.006), the induction of apoptosis (P<0.001), and the release of cytochrome C from mitochondria to the cytosolic fraction, thus activating caspase-9. These data suggest that over-expression of UCP2 has anti-apoptotic properties by inhibiting ROS-mediated apoptosis in A549 cells under hypoxic conditions.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenocarcinoma / genetics
  • Adenocarcinoma / metabolism
  • Adenocarcinoma / pathology
  • Adenocarcinoma of Lung
  • Apoptosis / drug effects*
  • Apoptosis / genetics
  • Cell Hypoxia / drug effects
  • Cell Hypoxia / genetics
  • Cell Hypoxia / physiology
  • Cell Line, Tumor
  • Cobalt / pharmacology
  • Down-Regulation / drug effects
  • Down-Regulation / genetics
  • Gene Expression
  • Gene Knockdown Techniques
  • Humans
  • Hypoxia-Inducible Factor 1, alpha Subunit / genetics
  • Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
  • Ion Channels / antagonists & inhibitors
  • Ion Channels / genetics
  • Ion Channels / physiology*
  • Lung Neoplasms / genetics
  • Lung Neoplasms / metabolism
  • Lung Neoplasms / pathology
  • Mitochondrial Proteins / antagonists & inhibitors
  • Mitochondrial Proteins / genetics
  • Mitochondrial Proteins / physiology*
  • Oxygen / pharmacology*
  • RNA, Small Interfering / pharmacology
  • Reactive Oxygen Species / metabolism
  • Reactive Oxygen Species / pharmacology*
  • Transfection
  • Uncoupling Protein 2

Substances

  • HIF1A protein, human
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Ion Channels
  • Mitochondrial Proteins
  • RNA, Small Interfering
  • Reactive Oxygen Species
  • UCP2 protein, human
  • Uncoupling Protein 2
  • Cobalt
  • cobaltous chloride
  • Oxygen