Blocking endogenous glypican-3 expression releases Hep 3B cells from G1 arrest.
Glypican-3 (GPC3) encodes a cell-surface heparan-sulfate proteoglycan mutated in type 1 Simpson-Golabi-Behmel syndrome (SGBS1), an X-linked overgrowth syndrome. The phenotype of SGBS1 patients and of GPC3 knockout mice suggests that GPC3 plays a negative role in cell proliferation, and an apoptosis-inducing role in specific tissues. Ectopic expression of GPC3 in some cell lines has supported the idea that GPC3 inhibits cell growth. Here we report that blocking endogenous GPC3 expression with an antisense transcript promotes the growth of Hep G2 and Hep 3B hepatoma cell lines. Moreover, antisense inhibition releases Hep 3B cells from cell cycle arrest. Hence, our data further support the notion that GPC3 is an inhibitor of cell proliferation and demonstrate that it modulates cell cycle progression.
Farooq
Mohammad
M
Department of Immunology, School of Medicine, Kyungpook National University, Daegu 700-422, Korea.
Hwang
Sun Young
SY
Park
Mi Kyung
MK
Kim
Jung-Chul
JC
Kim
Moon Kyu
MK
Sung
Young Kwan
YK
D000818:Animals; D006528:Carcinoma, Hepatocellular; D002455:Cell Division / Q000235:genetics*; D002460:Cell Line; D016193:G1 Phase; D053673:Glypicans; D019812:Heparan Sulfate Proteoglycans / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D006801:Humans; D008055:Lipids / Q000494:pharmacology; D051379:Mice; D016376:Oligonucleotides, Antisense / Q000494:pharmacology; D051381:Rats; D014407:Tumor Cells, Cultured
D053673:Glypicans; D019812:Heparan Sulfate Proteoglycans; D008055:Lipids; C086724:Lipofectamine; D016376:Oligonucleotides, Antisense