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Deleted in liver cancer 2 (DLC2) was dispensable for development and its deficiency did not aggravate

Tai On Yau1, Thomas Ho Yin Leung, Sandra Lam

  • 1Liver Cancer and Hepatitis Research Laboratory and SH Ho Foundation Research Laboratories, Department of Pathology, The University of Hong Kong, Hong Kong, China.

Plos One
|August 12, 2009
PubMed

Insights

Deleted in liver cancer 2 (DLC2) deficiency did not increase liver cancer in mice. DLC2-deficient mice showed reduced size and adipose tissue, suggesting DLC2 is not essential for hepatocarcinogenesis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Deleted in liver cancer 2 (DLC2) is a Rho GTPase-activating protein.
  • DLC2 is underexpressed in human hepatocellular carcinoma (HCC).
  • DLC2 exhibits tumor suppressor functions in cell culture models.

Purpose of the Study:

  • To investigate the in vivo tumor suppressor role of DLC2 in hepatocarcinogenesis.
  • To determine the function of DLC2 in vivo using a knockout mouse model.

Main Methods:

  • Generation of DLC2-deficient mice.
  • Assessment of embryonic development and survival.
  • Evaluation of spontaneous and diethylnitrosamine (DEN)-induced hepatocarcinogenesis.
  • Phenotypic analysis including body size and adipose tissue measurement.

Main Results:

  • DLC2 is dispensable for embryonic development; DLC2-deficient mice survive to adulthood.
  • No increased incidence of spontaneous or DEN-induced liver tumors was observed in DLC2-deficient mice.
  • DLC2-deficient mice exhibited smaller body size and reduced adipose tissue compared to wild-type littermates.
  • Observed phenotypes were not attributed to reduced cell size or adipogenesis defects.

Conclusions:

  • DLC2 deficiency alone does not enhance hepatocarcinogenesis.
  • DLC2 is not essential for liver tumor suppression in vivo.
  • DLC2 plays a role in regulating body size and adipose tissue, independent of its role in HCC.

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