Deleted in Liver Cancer 2 (DLC2) protein expression in hepatocellular carcinoma

Eur J Histochem. 2019 Feb 18;63(1):2981. doi: 10.4081/ejh.2019.2981.

Abstract

Deleted in Liver Cancer (DLC) proteins belong to the family of RhoGAPs and are believed to operate as negative regulators of the Rho family of small GTPases. So far, the role of the first identified member from the DLC family, DLC1, was established as a tumor suppressor in hepatocellular carcinoma. The function of its close family relative, DLC2 is unequivocal. In the present study we attempted to determine whether the loss of DLC2 is a common feature of hepatocellular carcinoma tissue. We examined two types of hepatocellular carcinoma- typical and fibrolamellar one. Our analysis revealed that DLC2 protein is not diminished in cancer tissue when compared to non-cancerous liver specimens. What is more, we observed DLC2 to be more abundantly expressed in cancer tissue, particularly in tumors with the inflammation background. In addition, we found that DLC2 gene status was diploid in virtually all tumor samples examined. Our results indicate that DLC2 is not diminished in hepatocellular carcinoma cells. It appears that members of the DLC family, although structurally highly related, may function differently in cancer cells.

MeSH terms

  • Carcinoma, Hepatocellular / genetics
  • Carcinoma, Hepatocellular / metabolism*
  • Diploidy
  • GTPase-Activating Proteins / genetics
  • GTPase-Activating Proteins / immunology
  • GTPase-Activating Proteins / metabolism*
  • Humans
  • Immunohistochemistry
  • Liver Neoplasms / genetics
  • Liver Neoplasms / metabolism*
  • Tumor Suppressor Proteins / genetics
  • Tumor Suppressor Proteins / immunology
  • Tumor Suppressor Proteins / metabolism*

Substances

  • GTPase-Activating Proteins
  • STARD13 protein, human
  • Tumor Suppressor Proteins

Grants and funding

Funding: The present work was supported by the grant no. 3509/B/P01/2010/38 from the Polish State Committee for Scientific Research and by the Medical University of Warsaw, funding no. 1M11/PM11.