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Article: RBMS3 at 3p24 inhibits nasopharyngeal carcinoma development via inhibiting cell proliferation, angiogenesis, and inducing apoptosis.

TitleRBMS3 at 3p24 inhibits nasopharyngeal carcinoma development via inhibiting cell proliferation, angiogenesis, and inducing apoptosis.
Authors
Issue Date2012
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
Citation
PLoS One, 2012, v. 7 n. 9, p. e44636 How to Cite?
AbstractDeletion of the short arm of chromosome 3 is one of the most frequent genetic alterations in many solid tumors including nasopharyngeal carcinoma (NPC), suggesting the existence of one or more tumor suppressor genes (TSGs) within the frequently deleted region. A putative TSG RBMS3 (RNA binding motif, single stranded interacting protein 3), located at 3p24-p23, has been identified in our previous study. Here, we reported that downregulation of RBMS3 was detected in 3/3 NPC cell lines and 13/15 (86.7%) primary NPC tissues. Functional studies using both overexpression and suppression systems demonstrated that RBMS3 has a strong tumor suppressive role in NPC. The tumor suppressive mechanism of RBMS3 was associated with its role in cell cycle arrest at the G1/S checkpoint by upregulating p53 and p21, downregulating cyclin E and CDK2, and the subsequent inhibition of Rb-ser780. Further analysis demonstrated that RBMS3 had a pro-apoptotic role in a mitochondrial-dependent manner via activation of caspase-9 and PARP. Finally, RBMS3 inhibited microvessel formation, which may be mediated by down-regulation of MMP2 and β-catenin and inactivation of its downstream targets, including cyclin-D1, c-Myc, MMP7, and MMP9. Taken together, our findings define a function for RBMS3 as an important tumor suppressor gene in NPC.
Persistent Identifierhttp://hdl.handle.net/10722/188984

 

DC FieldValueLanguage
dc.contributor.authorCHEN, Jen_US
dc.contributor.authorKwong, DLWen_US
dc.contributor.authorZHU, Cen_US
dc.contributor.authorChen, Len_US
dc.contributor.authorDong, Sen_US
dc.contributor.authorZHANG, Len_US
dc.contributor.authorTian, Jen_US
dc.contributor.authorQi, CBen_US
dc.contributor.authorCAO, Ten_US
dc.contributor.authorWONG, AMGen_US
dc.contributor.authorKong, KLen_US
dc.contributor.authorLi, Yen_US
dc.contributor.authorLIU, Men_US
dc.contributor.authorFu, Len_US
dc.contributor.authorGuan, Xen_US
dc.date.accessioned2013-09-17T14:22:30Z-
dc.date.available2013-09-17T14:22:30Z-
dc.date.issued2012en_US
dc.identifier.citationPLoS One, 2012, v. 7 n. 9, p. e44636en_US
dc.identifier.urihttp://hdl.handle.net/10722/188984-
dc.description.abstractDeletion of the short arm of chromosome 3 is one of the most frequent genetic alterations in many solid tumors including nasopharyngeal carcinoma (NPC), suggesting the existence of one or more tumor suppressor genes (TSGs) within the frequently deleted region. A putative TSG RBMS3 (RNA binding motif, single stranded interacting protein 3), located at 3p24-p23, has been identified in our previous study. Here, we reported that downregulation of RBMS3 was detected in 3/3 NPC cell lines and 13/15 (86.7%) primary NPC tissues. Functional studies using both overexpression and suppression systems demonstrated that RBMS3 has a strong tumor suppressive role in NPC. The tumor suppressive mechanism of RBMS3 was associated with its role in cell cycle arrest at the G1/S checkpoint by upregulating p53 and p21, downregulating cyclin E and CDK2, and the subsequent inhibition of Rb-ser780. Further analysis demonstrated that RBMS3 had a pro-apoptotic role in a mitochondrial-dependent manner via activation of caspase-9 and PARP. Finally, RBMS3 inhibited microvessel formation, which may be mediated by down-regulation of MMP2 and β-catenin and inactivation of its downstream targets, including cyclin-D1, c-Myc, MMP7, and MMP9. Taken together, our findings define a function for RBMS3 as an important tumor suppressor gene in NPC.-
dc.languageengen_US
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action-
dc.relation.ispartofPLoS Oneen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleRBMS3 at 3p24 inhibits nasopharyngeal carcinoma development via inhibiting cell proliferation, angiogenesis, and inducing apoptosis.en_US
dc.typeArticleen_US
dc.identifier.emailKwong, DLW: dlwkwong@hku.hken_US
dc.identifier.emailChen, L: pollyllc@hku.hken_US
dc.identifier.emailDong, S: dongss@hku.hken_US
dc.identifier.emailKong, KL: karlok@hku.hken_US
dc.identifier.emailLi, Y: vikkiyan@hku.hken_US
dc.identifier.emailFu, L: gracefu@graduate.hku.hken_US
dc.identifier.emailGuan, X: xyguan@hkucc.hku.hken_US
dc.identifier.authorityKwong, DLW=rp00414en_US
dc.identifier.authorityFu, L=rp01435en_US
dc.identifier.authorityGuan, X=rp00454en_US
dc.description.naturepublished_or_final_version-
dc.identifier.hkuros224317en_US
dc.identifier.volume7en_US
dc.identifier.issue9en_US
dc.identifier.spagee44636en_US
dc.identifier.epagee44636en_US

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