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Article: PTPRG suppresses tumor growth and invasion via inhibition of Akt signaling in nasopharyngeal carcinoma

TitlePTPRG suppresses tumor growth and invasion via inhibition of Akt signaling in nasopharyngeal carcinoma
Authors
Issue Date2015
PublisherImpact Journals LLC. The Journal's web site is located at http://www.impactjournals.com/oncotarget/index.html
Citation
Oncotarget, 2015, v. 6 n. 15, p. 13434-13447 How to Cite?
AbstractProtein Tyrosine Phosphatase, Receptor Type G (PTPRG) was identified as a candidate tumor suppressor gene in nasopharyngeal carcinoma (NPC). PTPRG induces significant in vivo tumor suppression in NPC. We identified EGFR as a PTPRG potential interacting partner and examined this interaction. Dephosphorylation of EGFR at EGFR-Y1068 and -Y1086 sites inactivated the PI3K/Akt signaling cascade and subsequent down-regulation of downstream pro-angiogenic and -invasive proteins (VEGF, IL6, and IL8) and suppressed tumor cell proliferation, angiogenesis, and invasion. The effect of Akt inhibition in NPC cells was further validated by Akt knockdown experiments in the PTPRG-down-regulated NPC cell lines. Our results suggested that inhibition of Akt in NPC cells induces tumor suppression at both the in vitro and in vivo levels, and also importantly, in vivo metastasis. In conclusion, we confirmed the vital role of PTPRG in inhibiting Akt signaling with the resultant suppression of in vivo tumorigenesis and metastasis.
Persistent Identifierhttp://hdl.handle.net/10722/211739
ISSN
2015 Impact Factor: 5.008
2015 SCImago Journal Rankings: 2.294

 

DC FieldValueLanguage
dc.contributor.authorCheung, AKL-
dc.contributor.authorIp, JCY-
dc.contributor.authorChu, ACH-
dc.contributor.authorCheng, Y-
dc.contributor.authorLeong, MML-
dc.contributor.authorKo, JMY-
dc.contributor.authorShuen, WH-
dc.contributor.authorLung, HL-
dc.contributor.authorLung, ML-
dc.date.accessioned2015-07-21T02:09:39Z-
dc.date.available2015-07-21T02:09:39Z-
dc.date.issued2015-
dc.identifier.citationOncotarget, 2015, v. 6 n. 15, p. 13434-13447-
dc.identifier.issn1949-2553-
dc.identifier.urihttp://hdl.handle.net/10722/211739-
dc.description.abstractProtein Tyrosine Phosphatase, Receptor Type G (PTPRG) was identified as a candidate tumor suppressor gene in nasopharyngeal carcinoma (NPC). PTPRG induces significant in vivo tumor suppression in NPC. We identified EGFR as a PTPRG potential interacting partner and examined this interaction. Dephosphorylation of EGFR at EGFR-Y1068 and -Y1086 sites inactivated the PI3K/Akt signaling cascade and subsequent down-regulation of downstream pro-angiogenic and -invasive proteins (VEGF, IL6, and IL8) and suppressed tumor cell proliferation, angiogenesis, and invasion. The effect of Akt inhibition in NPC cells was further validated by Akt knockdown experiments in the PTPRG-down-regulated NPC cell lines. Our results suggested that inhibition of Akt in NPC cells induces tumor suppression at both the in vitro and in vivo levels, and also importantly, in vivo metastasis. In conclusion, we confirmed the vital role of PTPRG in inhibiting Akt signaling with the resultant suppression of in vivo tumorigenesis and metastasis.-
dc.languageeng-
dc.publisherImpact Journals LLC. The Journal's web site is located at http://www.impactjournals.com/oncotarget/index.html-
dc.relation.ispartofOncotarget-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titlePTPRG suppresses tumor growth and invasion via inhibition of Akt signaling in nasopharyngeal carcinoma-
dc.typeArticle-
dc.identifier.emailCheung, AKL: arthurhk@hku.hk-
dc.identifier.emailIp, JCY: josephip@hku.hk-
dc.identifier.emailChu, ACH: adrianac@HKUCC-COM.hku.hk-
dc.identifier.emailCheng, Y: yuecheng@HKUCC-COM.hku.hk-
dc.identifier.emailLeong, MML: merrin@hku.hk-
dc.identifier.emailKo, JMY: joko@hku.hk-
dc.identifier.emailLung, HL: hllung2@hku.hk-
dc.identifier.emailLung, ML: mlilung@hku.hk-
dc.identifier.authorityCheung, AKL=rp01769-
dc.identifier.authorityCheng, Y=rp01320-
dc.identifier.authorityKo, JMY=rp02011-
dc.identifier.authorityLung, HL=rp00299-
dc.identifier.authorityLung, ML=rp00300-
dc.description.naturepublished_or_final_version-
dc.identifier.pmid25970784-
dc.identifier.hkuros244772-
dc.identifier.volume6-
dc.identifier.issue15-
dc.identifier.spage13434-
dc.identifier.epage13447-
dc.publisher.placeUnited States-

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