[The association between signal-regulatory protein alpha and hepatocellular carcinoma]

Zhonghua Yi Xue Za Zhi. 1999 Apr;79(4):268-70.
[Article in Chinese]

Abstract

Objective: To study the roles of signal-regulatory protein alpha (SIRP alpha) in the development of hepatocellular carcinoma (HCC).

Methods: 42 pairs of HCC and the surrounding noncancerous hepatic tissues were used. The expression of SIRP alpha in various tissues was determined by Northern blot analysis and immunohistochemistry assay, by which together with the pathologic characteristics of each sample, the role of SIRP alpha was investigated.

Results: The expression of SIRP alpha significantly decreased in 21 cases of samples (50.0%) to the 3.9 kb transcript and 27 cases of samples (64.3%) to the 2.5 kb transcript respectively. The SIRP alpha decreasing rate in large HCC(> 5 cm in diameter) was higher than in small HCC (< or = 5 cm in diameter), and in HCC with cancer embolus was higher than that of without cancer embolus. No association was found between the SIRP alpha expression and the patient's age, tumor grade, tumor capsule, serum AFP level, and HBV infection. Immunohistochemistry showed that all the normal hepatocytes, cholangioepithelial cells, Ito cells, regenerated hepatocytes, new generated cholangioepithelial cells and part of HCC cells were positive. The HCC tissues in which SIRP alpha was down-regulated showed positive particles becoming weaker and less, and some tumor cells and area were completely negative.

Conclusion: The expression of SIRP alpha especially 2.5 kb transcript is down-regulated in HCC, which is closely related with the tumor growth and invasiveness. SIRP alpha may be an important negative regulator of HCC.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antigens, Differentiation*
  • Carcinoma, Hepatocellular / metabolism*
  • Carcinoma, Hepatocellular / pathology
  • Down-Regulation
  • Humans
  • Liver Neoplasms / metabolism*
  • Liver Neoplasms / pathology
  • Membrane Glycoproteins / metabolism*
  • Neural Cell Adhesion Molecule L1*
  • Neural Cell Adhesion Molecules / metabolism*
  • Receptors, Immunologic*
  • Signal Transduction*

Substances

  • Antigens, Differentiation
  • Membrane Glycoproteins
  • Neural Cell Adhesion Molecule L1
  • Neural Cell Adhesion Molecules
  • Receptors, Immunologic