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Article: Calcium-binding protein 39 promotes hepatocellular carcinoma growth and metastasis by activating extracellular signal-regulated kinase signaling pathway

TitleCalcium-binding protein 39 promotes hepatocellular carcinoma growth and metastasis by activating extracellular signal-regulated kinase signaling pathway
Authors
Issue Date2017
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/
Citation
Hepatology, 2017, v. 66 n. 5, p. 1529-1545 How to Cite?
AbstractCalcium binding protein (CAB39) is a key regulator of a group of STE20 kinases. Here we report that CAB39 was frequently up-regulated in hepatocellular carcinoma (HCC), which was significantly associated with tumor metastasis (P=0.000), poorer diseasefree survival rate (P=0.027) and poor prognosis (P=0.000). Ectopic expression of CAB39 in immortalized human liver cell line LO2 and HCC cell lines QGY-7703 and BEL-7402 could increase foci formation, colony formation in soft agar, tumor formation in nude mice and cell motility. Silencing CAB39 expression in two HCC cell lines Huh7 and MHCC97H with short hairpin RNA could effectively abolish its oncogenic function. Further study found that CAB39 contributed to the ERK pathway activation and mutations of the key sites of CAB39 markedly decrease the level of the phosphorylated ERK. In addition, CAB39 could promote epithelial-mesenchymal transition (EMT) by up-regulating N-cadherin and Fibronectin, and down-regulating Ecadherin and α-E-catenin. As a result, β-catenin nuclear translocation was increased and its downstream target gene MMP-9 was up-regulated. Taken together, our findings suggested that CAB39 play very important oncogenic roles in HCC pathogenesis and progression by activating ERK signaling pathway. Better understanding of CAB39 may lead to its clinical application as a biomarker for prognosis predictor and a novel therapeutic target.
Persistent Identifierhttp://hdl.handle.net/10722/243063
ISSN
2017 Impact Factor: 14.079
2015 SCImago Journal Rankings: 4.752
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorJiang, L-
dc.contributor.authorLiu, M-
dc.contributor.authorLi, Y-
dc.contributor.authorKwong, DLW-
dc.contributor.authorGuan, X-
dc.date.accessioned2017-08-25T02:49:26Z-
dc.date.available2017-08-25T02:49:26Z-
dc.date.issued2017-
dc.identifier.citationHepatology, 2017, v. 66 n. 5, p. 1529-1545-
dc.identifier.issn0270-9139-
dc.identifier.urihttp://hdl.handle.net/10722/243063-
dc.description.abstractCalcium binding protein (CAB39) is a key regulator of a group of STE20 kinases. Here we report that CAB39 was frequently up-regulated in hepatocellular carcinoma (HCC), which was significantly associated with tumor metastasis (P=0.000), poorer diseasefree survival rate (P=0.027) and poor prognosis (P=0.000). Ectopic expression of CAB39 in immortalized human liver cell line LO2 and HCC cell lines QGY-7703 and BEL-7402 could increase foci formation, colony formation in soft agar, tumor formation in nude mice and cell motility. Silencing CAB39 expression in two HCC cell lines Huh7 and MHCC97H with short hairpin RNA could effectively abolish its oncogenic function. Further study found that CAB39 contributed to the ERK pathway activation and mutations of the key sites of CAB39 markedly decrease the level of the phosphorylated ERK. In addition, CAB39 could promote epithelial-mesenchymal transition (EMT) by up-regulating N-cadherin and Fibronectin, and down-regulating Ecadherin and α-E-catenin. As a result, β-catenin nuclear translocation was increased and its downstream target gene MMP-9 was up-regulated. Taken together, our findings suggested that CAB39 play very important oncogenic roles in HCC pathogenesis and progression by activating ERK signaling pathway. Better understanding of CAB39 may lead to its clinical application as a biomarker for prognosis predictor and a novel therapeutic target.-
dc.languageeng-
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/-
dc.relation.ispartofHepatology-
dc.rightsHepatology. Copyright © John Wiley & Sons, Inc.-
dc.rightsPreprint: This is the pre-peer reviewed version of the following article: [FULL CITE], which has been published in final form at [Link to final article using the DOI]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving. Postprint: This is the peer reviewed version of the following article: [FULL CITE], which has been published in final form at [Link to final article using the DOI]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving. Special Statement for Preprint only Before publication: 'This is a preprint of an article accepted for publication in [The Journal of Pathology] Copyright © ([year]) ([Pathological Society of Great Britain and Ireland])'. After publication: the preprint notice should be amended to follows: 'This is a preprint of an article published in [include the complete citation information for the final version of the Contribution as published in the print edition of the Journal]' For Cochrane Library/ Cochrane Database of Systematic Reviews, add statement & acknowledgement : ‘This review is published as a Cochrane Review in the Cochrane Database of Systematic Reviews 20XX, Issue X. Cochrane Reviews are regularly updated as new evidence emerges and in response to comments and criticisms, and the Cochrane Database of Systematic Reviews should be consulted for the most recent version of the Review.’ Please include reference to the Review and hyperlink to the original version using the following format e.g. Authors. Title of Review. Cochrane Database of Systematic Reviews 20XX, Issue #. Art. No.: CD00XXXX. DOI: 10.1002/14651858.CD00XXXX (insert persistent link to the article by using the URL: http://dx.doi.org/10.1002/14651858.CD00XXXX) (This statement should refer to the most recent issue of the Cochrane Database of Systematic Reviews in which the Review published.)-
dc.titleCalcium-binding protein 39 promotes hepatocellular carcinoma growth and metastasis by activating extracellular signal-regulated kinase signaling pathway-
dc.typeArticle-
dc.identifier.emailJiang, L: lxjiang@hku.hk-
dc.identifier.emailKwong, DLW: dlwkwong@hku.hk-
dc.identifier.emailGuan, X: xyguan@hkucc.hku.hk-
dc.identifier.authorityKwong, DLW=rp00414-
dc.identifier.authorityGuan, X=rp00454-
dc.identifier.doi10.1002/hep.29312-
dc.identifier.hkuros275234-
dc.identifier.volume66-
dc.identifier.issue5-
dc.identifier.spage1529-
dc.identifier.epage1545-
dc.identifier.isiWOS:000436963800017-
dc.publisher.placeUnited States-

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