Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 손장원 | - |
dc.date.accessioned | 2018-03-05T00:53:38Z | - |
dc.date.available | 2018-03-05T00:53:38Z | - |
dc.date.issued | 2013-10 | - |
dc.identifier.citation | PLOS ONE,20132,8(10),p | en_US |
dc.identifier.issn | 1932-6203 | - |
dc.identifier.uri | http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0076895 | - |
dc.identifier.uri | http://hdl.handle.net/20.500.11754/42056 | - |
dc.description.abstract | G-protein-coupled receptors (GPCR) are the largest family of cell surface molecules that play important role/s in a number of biological and pathological processes including cancers. Earlier studies have highlighted the importance of Wnt7a signaling via its cognate receptor Frizzled9, a GPCR, in inhibition of cell proliferation, anchorage-independent growth, and reversal of transformed phenotype in non small cell lung cancer primarily through activation of the tumor suppressor, PPAR gamma. However, the G-protein effectors that couple to this important tumor suppressor pathway have not been identified, and are of potential therapeutic interest. In this study, by using two independent Wnt7a/Frizzled9-specific read-outs, we identify G(alpha 16) as a novel downstream effector of Wnt7a/Frizzled9 signaling. Interestingly, G(alpha 16) expression is severely down-regulated, both at the messenger RNA levels and protein levels, in many non small cell lung cancer cell lines. Additionally, through gene-specific knock-downs and expression of GTPase-deficient forms (Q212L) of G(alpha 16), we also establish G(alpha 16) as a novel regulator of non small cell lung cancer cell proliferation and anchorage-independent cell growth. Taken together, our data not only establish the importance of G(alpha 16) as a critical downstream effector of the non-canonical Wnt signaling pathway but also as a potential therapeutic target for the treatment of non small cell lung cancer. | en_US |
dc.description.sponsorship | U.S. Department of Veterans Affairs, National Institutes of Health (NIH) | en_US |
dc.language.iso | en | en_US |
dc.publisher | PUBLIC LIBRARY SCIENCE, 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA | en_US |
dc.subject | ACTIVATED-RECEPTOR-GAMMA | en_US |
dc.subject | EPITHELIAL-MESENCHYMAL TRANSITIONS | en_US |
dc.subject | COUPLED RECEPTORS | en_US |
dc.subject | TERATOCARCINOMA CELLS | en_US |
dc.subject | RAT FRIZZLED-1 | en_US |
dc.subject | TCF PATHWAY | en_US |
dc.subject | CYCLIC-GMP | en_US |
dc.subject | KINASE | en_US |
dc.subject | EXPRESSION | en_US |
dc.subject | TRANSDUCTION | en_US |
dc.title | Heterotrimeric G-Protein, G(alpha 16), Is a Critical Downstream Effector of Non-Canonical Wnt Signaling and a Potent Inhibitor of Transformed Cell Growth in Non Small Cell Lung Cancer | en_US |
dc.type | Article | en_US |
dc.relation.no | 10 | - |
dc.relation.volume | 8 | - |
dc.identifier.doi | 10.1371/journal.pone.0076895 | - |
dc.relation.page | 1-10 | - |
dc.relation.journal | PLOS ONE | - |
dc.contributor.googleauthor | Avasarala, Sreedevi | - |
dc.contributor.googleauthor | Bikkavilli, Rama Kamesh | - |
dc.contributor.googleauthor | Van Scoyk, Michelle | - |
dc.contributor.googleauthor | Zhang, Wei | - |
dc.contributor.googleauthor | Lapite, Ajibike | - |
dc.contributor.googleauthor | Hostetter, Logan | - |
dc.contributor.googleauthor | Byers, Joshua T. | - |
dc.contributor.googleauthor | Heasley, Lynn E. | - |
dc.contributor.googleauthor | Sohn, Jang Won | - |
dc.contributor.googleauthor | Winn, Robert A. | - |
dc.relation.code | 2013007124 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | jwsohn | - |
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