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Article: TP53INP1 downregulation activates a p73-dependent DUSP10/ERK signaling pathway to promote metastasis of hepatocellular carcinoma

TitleTP53INP1 downregulation activates a p73-dependent DUSP10/ERK signaling pathway to promote metastasis of hepatocellular carcinoma
Authors
Issue Date2017
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
Cancer Research, 2017, v. 77 n. 17, p. 4602-4612 How to Cite?
AbstractIdentifying critical factors involved in the metastatic progression of hepatocellular carcinoma (HCC) may offer important therapeutic opportunities. Here, we report that the proapoptotic stress response factor TP53INP1 is often selectively downregulated in advanced stage IV and metastatic human HCC tumors. Mechanistic investigations revealed that TP53INP1 downregulation in early-stage HCC cells promoted metastasis via DUSP10 phosphatase-mediated activation of the ERK pathway. The DUSP10 promoter included putative binding sites for p73 directly implicated in modulation by TP53INP1. Overall, our findings show how TP53INP1 plays a critical role in limiting the progression of early-stage HCC, with implications for developing new therapeutic strategies to attack metastatic HCC.
Persistent Identifierhttp://hdl.handle.net/10722/242935
ISSN
2023 Impact Factor: 12.5
2023 SCImago Journal Rankings: 3.468
ISI Accession Number ID
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DC FieldValueLanguage
dc.contributor.authorNg, KY-
dc.contributor.authorChan, LH-
dc.contributor.authorChai, S-
dc.contributor.authorTong, M-
dc.contributor.authorGuan, X-
dc.contributor.authorLee, PY-
dc.contributor.authorYuan, Y-
dc.contributor.authorXie, D-
dc.contributor.authorLee, TK-
dc.contributor.authorDusetti, NJ-
dc.contributor.authorCarrier, A-
dc.contributor.authorMa, SKY-
dc.date.accessioned2017-08-25T02:47:33Z-
dc.date.available2017-08-25T02:47:33Z-
dc.date.issued2017-
dc.identifier.citationCancer Research, 2017, v. 77 n. 17, p. 4602-4612-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/242935-
dc.description.abstractIdentifying critical factors involved in the metastatic progression of hepatocellular carcinoma (HCC) may offer important therapeutic opportunities. Here, we report that the proapoptotic stress response factor TP53INP1 is often selectively downregulated in advanced stage IV and metastatic human HCC tumors. Mechanistic investigations revealed that TP53INP1 downregulation in early-stage HCC cells promoted metastasis via DUSP10 phosphatase-mediated activation of the ERK pathway. The DUSP10 promoter included putative binding sites for p73 directly implicated in modulation by TP53INP1. Overall, our findings show how TP53INP1 plays a critical role in limiting the progression of early-stage HCC, with implications for developing new therapeutic strategies to attack metastatic HCC.-
dc.languageeng-
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/-
dc.relation.ispartofCancer Research-
dc.titleTP53INP1 downregulation activates a p73-dependent DUSP10/ERK signaling pathway to promote metastasis of hepatocellular carcinoma-
dc.typeArticle-
dc.identifier.emailNg, KY: jkyng@hku.hk-
dc.identifier.emailTong, M: caroltm@hku.hk-
dc.identifier.emailGuan, X: xyguan@hkucc.hku.hk-
dc.identifier.emailLee, PY: nikkilee@hku.hk-
dc.identifier.emailMa, SKY: stefma@hku.hk-
dc.identifier.authorityTong, M=rp02568-
dc.identifier.authorityGuan, X=rp00454-
dc.identifier.authorityLee, PY=rp00263-
dc.identifier.authorityMa, SKY=rp00506-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1158/0008-5472.CAN-16-3456-
dc.identifier.pmid28674078-
dc.identifier.scopuseid_2-s2.0-85028831453-
dc.identifier.hkuros274872-
dc.identifier.hkuros288916-
dc.identifier.volume77-
dc.identifier.issue17-
dc.identifier.spage4602-
dc.identifier.epage4612-
dc.identifier.isiWOS:000409030100008-
dc.publisher.placeUnited States-
dc.relation.projectA Multidisciplinary Study on CD133 Liver Cancer Stem Cells: Molecular Mechanisms, Clinical Relevance and Therapeutic Implications-
dc.identifier.issnl0008-5472-

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