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DLC-1, a GTPase-activating protein for Rho, is associated with cell proliferation, morphology, and migration in human hepatocellular carcinoma

Cited 65 time in Web of Science Cited 65 time in Scopus
Authors
Kim, Tai Young; Lee, Jung Weon; Kim, Hwang-Phill; Jong, Hyun-Soon; Kim, Tae-You; Jung, Mira; Bang, Yung-Jue
Issue Date
2007
Publisher
Elsevier
Citation
Biochem. Biophys. Res. Commun. 355 (2007) 72-77
Keywords
Carcinoma, Hepatocellular/metabolism/*pathologyCell DivisionCell LineCell Line, TumorCell MovementHumansKidneyLiver Neoplasms/metabolism/*pathologyMutagenesis, Site-DirectedPhosphoproteins/metabolismPolymerase Chain ReactionRNA, Messenger/geneticsRecombinant Proteins/metabolismTumor Suppressor Proteins/*genetics/metabolism
Abstract
DLC-1 (deleted in liver cancer-1) is a tumor suppressor gene for hepatocellular carcinoma and other cancers. To characterize its functions, we constructed recombinant adenovirus encoding the wild-type DLC-1 and examined its effects on behaviors of a hepatocellular carcinoma cell line (SNU-368), which does not express DLC-1. Here, we found that restoration of DLC-1 expression in the SNU-368 cells caused an inhibition of cell proliferation with an increase of a subG1 population. Furthermore, DLC-1 overexpression induced disassembly of stress fibers and extensive membrane protrusions around cells on laminin-1. DLC-1 overexpression also inhibited cell migration and dephosphorylated focal adhesion proteins such as focal adhesion kinase (FAK), Cas (p130Cas; Crk-associated substrate), and paxillin. These observations suggest that DLC-1 plays important roles in signal transduction pathway regulating cell proliferation, cell morphology, and cell migration by affecting Rho family GTPases and focal adhesion proteins.
ISSN
0006-291X (Print)
Language
English
URI
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WBK-4MY0S1B-3&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=453d0b8262d72c34c22b3e72d7df9338

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17292327

http://hdl.handle.net/10371/23281
DOI
https://doi.org/10.1016/j.bbrc.2007.01.121
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College of Medicine/School of Medicine (의과대학/대학원)Program in Cancer Biology (협동과정-종양생물학전공)Journal Papers (저널논문_협동과정-종양생물학전공)
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