Exp Mol Med.
2003 Aug;35(4):257-262.
Growth promotion of HepG2 hepatoma cells by antisense-mediated knockdown of glypican-3 is independent of insulin-like growth factor 2 signaling
- Affiliations
-
- 1Department of Immunology, Medical School, Kyungpook National University, Daegu 700-422, Korea. moonkim@knu.ac.kr
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.
- Full Text Links
-
- Actions
-
Cited
- CITED
-
- Close
- Share
-
- Similar articles
-
- The Effect of Insulin and Epidermal Growth Factor on the Proliferation of Endometrial Carcinoma Cell Line
- Relationship of Insulin like Growth Factor I with Pharmacologically Stimulated Growth Hormone Secretion in Growth Hormone Deficient Children
- Correlation between Retinoic Acid Sensitivity and IGFBP-3, AFP Protein Expression in Hepatoma Cell Lines
- The Effects of TGF-beta2 and bFGF on the Proliferation of Retinal Pigment Epithelial Cells
- IGF-I Exerts an Anti-inflammatory Effect on Skeletal Muscle Cells through Down-regulation of TLR4 Signaling
