title: Blocking endogenous glypican-3 expression releases Hep 3B cells from G1 arrest.
abstract: 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.
authors.affiliation: Department of Immunology, School of Medicine, Kyungpook National University, Daegu 700-422, Korea.
authors.forename: Mohammad
authors.initials: M
authors.lastname: Farooq
authors.forename: Sun Young
authors.initials: SY
authors.lastname: Hwang
authors.forename: Mi Kyung
authors.initials: MK
authors.lastname: Park
authors.forename: Jung-Chul
authors.initials: JC
authors.lastname: Kim
authors.forename: Moon Kyu
authors.initials: MK
authors.lastname: Kim
authors.forename: Young Kwan
authors.initials: YK
authors.lastname: Sung
mesh_terms: 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
chemical_list: D053673:Glypicans; D019812:Heparan Sulfate Proteoglycans; D008055:Lipids; C086724:Lipofectamine; D016376:Oligonucleotides, Antisense