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Article: Maelstrom promotes hepatocellular carcinoma metastasis by inducing epithelial-mesenchymal transition by way of Akt/GSK-3β/ Snail signaling

TitleMaelstrom promotes hepatocellular carcinoma metastasis by inducing epithelial-mesenchymal transition by way of Akt/GSK-3β/ Snail signaling
Authors
Issue Date2014
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/
Citation
Hepatology, 2014, v. 59 n. 2, p. 531-543 How to Cite?
AbstractAmplification of 1q is one of the most frequent chromosomal alterations in human hepatocellular carcinoma (HCC). In this study we identified and characterized a novel oncogene, Maelstrom (MAEL), at 1q24. Amplification and overexpression of MAEL was frequently detected in HCCs and significantly associated with HCC recurrence (P = 0.031) and poor outcome (P = 0.001). Functional study demonstrated that MAEL promoted cell growth, cell migration, and tumor formation in nude mice, all of which were effectively inhibited when MAEL was silenced with short hairpin RNA (shRNAs). Further study found that MAEL enhanced AKT activity with subsequent GSK-3beta phosphorylation and Snail stabilization, finally inducing epithelial-mesenchymal transition (EMT) and promoting tumor invasion and metastasis. In addition, MAEL up-regulated various stemness-related genes, multidrug resistance genes, and cancer stem cell (CSC) surface markers at the messenger RNA (mRNA) level. Functional study demonstrated that overexpression of MAEL increased self-renewal, chemoresistance, and tumor metastasis. CONCLUSION: MAEL is an oncogene that plays an important role in the development and progression of HCC by inducing EMT and enhancing the stemness of HCC.
Persistent Identifierhttp://hdl.handle.net/10722/198984
ISSN
2015 Impact Factor: 11.711
2015 SCImago Journal Rankings: 4.752
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLiu, L-
dc.contributor.authorDai, Y-
dc.contributor.authorCHEN, J-
dc.contributor.authorZeng, T-
dc.contributor.authorLi, Y-
dc.contributor.authorChen, L-
dc.contributor.authorZhu, YH-
dc.contributor.authorLi, J-
dc.contributor.authorLi, Y-
dc.contributor.authorMa, SKY-
dc.contributor.authorXie, D-
dc.contributor.authorYuan, YF-
dc.contributor.authorGuan, X-
dc.date.accessioned2014-07-22T00:58:52Z-
dc.date.available2014-07-22T00:58:52Z-
dc.date.issued2014-
dc.identifier.citationHepatology, 2014, v. 59 n. 2, p. 531-543-
dc.identifier.issn0270-9139-
dc.identifier.urihttp://hdl.handle.net/10722/198984-
dc.description.abstractAmplification of 1q is one of the most frequent chromosomal alterations in human hepatocellular carcinoma (HCC). In this study we identified and characterized a novel oncogene, Maelstrom (MAEL), at 1q24. Amplification and overexpression of MAEL was frequently detected in HCCs and significantly associated with HCC recurrence (P = 0.031) and poor outcome (P = 0.001). Functional study demonstrated that MAEL promoted cell growth, cell migration, and tumor formation in nude mice, all of which were effectively inhibited when MAEL was silenced with short hairpin RNA (shRNAs). Further study found that MAEL enhanced AKT activity with subsequent GSK-3beta phosphorylation and Snail stabilization, finally inducing epithelial-mesenchymal transition (EMT) and promoting tumor invasion and metastasis. In addition, MAEL up-regulated various stemness-related genes, multidrug resistance genes, and cancer stem cell (CSC) surface markers at the messenger RNA (mRNA) level. Functional study demonstrated that overexpression of MAEL increased self-renewal, chemoresistance, and tumor metastasis. CONCLUSION: MAEL is an oncogene that plays an important role in the development and progression of HCC by inducing EMT and enhancing the stemness of HCC.-
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.rightsSpecial 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.subject.meshCarcinoma, Hepatocellular - physiopathology-
dc.subject.meshCarrier Proteins - genetics - physiology-
dc.subject.meshEpithelial-Mesenchymal Transition - physiology-
dc.subject.meshGlycogen Synthase Kinase 3 - physiology-
dc.subject.meshLiver Neoplasms - physiopathology-
dc.titleMaelstrom promotes hepatocellular carcinoma metastasis by inducing epithelial-mesenchymal transition by way of Akt/GSK-3β/ Snail signaling-
dc.typeArticle-
dc.identifier.emailLi, Y: vikkiyan@hku.hk-
dc.identifier.emailChen, L: pollyllc@hku.hk-
dc.identifier.emailMa, SKY: stefma@hku.hk-
dc.identifier.emailGuan, X: xyguan@hkucc.hku.hk-
dc.identifier.authorityMa, SKY=rp00506-
dc.identifier.authorityGuan, X=rp00454-
dc.identifier.doi10.1002/hep.26677-
dc.identifier.pmid23929794-
dc.identifier.scopuseid_2-s2.0-84893640620-
dc.identifier.hkuros231388-
dc.identifier.volume59-
dc.identifier.issue2-
dc.identifier.spage531-
dc.identifier.epage543-
dc.identifier.isiWOS:000330310300020-
dc.publisher.placeUnited States-

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