Growth promotion of HepG2 hepatoma cells by antisense-mediated knockdown of glypican-3 is independent of insulin-like growth factor 2 signaling.
- Author:
Young Kwan SUNG
1
;
Sung Young HWANG
;
Mohammad FAROOQ
;
Jung Chul KIM
;
Moon Kyu KIM
Author Information
1. Department of Immunology, Medical School, Kyungpook National University, Daegu 700-422, Korea. moonkim@knu.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
glypican-3;
growth suppression;
hepatoma;
insulin-like growth factor 2
- MeSH:
Carcinoma, Hepatocellular/*metabolism;
Growth Substances/*metabolism;
Heparan Sulfate Proteoglycan/*metabolism;
Human;
Insulin-Like Growth Factor II/*metabolism;
RNA, Antisense;
Signal Transduction/physiology
- From:Experimental & Molecular Medicine
2003;35(4):257-262
- CountryRepublic of Korea
- Language:English
-
Abstract:
Glypican-3 (GPC3) encodes a cell-surface heparan-sulfate proteoglycan and its expression is frequently silenced in ovarian cancer, mesotheliomas, and breast cancer cell lines and ectopic expression of GPC3 inhibited the growth of these cells, suggesting that GPC3 plays a negative role in cell proliferation. In contrast, up-regulation of GPC3 is often observed in hepatoma, neuroblastoma, and Wilms' tumor. Whether GPC3 plays the same growth inhibitory role in these tumors remains to be studied. Here we report that antisense-mediated knockdown of GPC3 in the HepG2 hepatoma cells significantly promotes the growth of hepatoma cells. In addition, we show that this growth promotion is independent of insulin-like growth factor 2 (IGF2) signaling. Our data suggest that GPC3 plays a growth-suppressing role in hepatoma and provide cell biological evidence inconsistent with the hypothesis that GPC3 acts as a growth suppressor by downregulating IGF2.
