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Article: ANXA3/JNK Signaling Promotes Self-Renewal and Tumor Growth, and Its Blockade Provides a Therapeutic Target for Hepatocellular Carcinoma

TitleANXA3/JNK Signaling Promotes Self-Renewal and Tumor Growth, and Its Blockade Provides a Therapeutic Target for Hepatocellular Carcinoma
Authors
Issue Date2015
PublisherElsevier (Cell Press): OAJ.
Citation
Stem Cell Reports, 2015, v. 5 n. 1, p. 45-59 How to Cite?
AbstractFrequent tumor relapse in hepatocellular carcinoma (HCC) has been commonly attributed to the presence of residual cancer stem cells (CSCs) after conventional treatments. We have previously identified and characterized CD133 to mark a specific CSC subset in HCC. In the present study, we found endogenous and secretory annexin A3 (ANXA3) to play pivotal roles in promoting cancer and stem cell-like features in CD133+ liver CSCs through a dysregulated JNK pathway. Blockade of ANXA3 with an anti-ANXA3 monoclonal antibody in vitro as well as in human HCC xenograft models resulted in a significant reduction in tumor growth and self-renewal. Clinically, ANXA3 expression in HCC patient sera closely associated with aggressive clinical features. Our results suggest that ANXA3 can serve as a novel diagnostic biomarker and that the inhibition of ANXA3 may be a viable therapeutic option for the treatment of CD133+ liver-CSC-driven HCC. © 2015 The Authors.
Persistent Identifierhttp://hdl.handle.net/10722/211613
ISSN
2015 Impact Factor: 7.023
2015 SCImago Journal Rankings: 5.523
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorTong, M-
dc.contributor.authorFung, TM-
dc.contributor.authorLuk, TCS-
dc.contributor.authorNg, KY-
dc.contributor.authorLee, KW-
dc.contributor.authorLin, C-
dc.contributor.authorYam, JWP-
dc.contributor.authorChan, KW-
dc.contributor.authorNg, F-
dc.contributor.authorZheng, B-
dc.contributor.authorYuan, YF-
dc.contributor.authorXie, D-
dc.contributor.authorLo, CM-
dc.contributor.authorMan, K-
dc.contributor.authorGuan, X-
dc.contributor.authorMa, SKY-
dc.date.accessioned2015-07-21T02:04:46Z-
dc.date.available2015-07-21T02:04:46Z-
dc.date.issued2015-
dc.identifier.citationStem Cell Reports, 2015, v. 5 n. 1, p. 45-59-
dc.identifier.issn2213-6711-
dc.identifier.urihttp://hdl.handle.net/10722/211613-
dc.description.abstractFrequent tumor relapse in hepatocellular carcinoma (HCC) has been commonly attributed to the presence of residual cancer stem cells (CSCs) after conventional treatments. We have previously identified and characterized CD133 to mark a specific CSC subset in HCC. In the present study, we found endogenous and secretory annexin A3 (ANXA3) to play pivotal roles in promoting cancer and stem cell-like features in CD133+ liver CSCs through a dysregulated JNK pathway. Blockade of ANXA3 with an anti-ANXA3 monoclonal antibody in vitro as well as in human HCC xenograft models resulted in a significant reduction in tumor growth and self-renewal. Clinically, ANXA3 expression in HCC patient sera closely associated with aggressive clinical features. Our results suggest that ANXA3 can serve as a novel diagnostic biomarker and that the inhibition of ANXA3 may be a viable therapeutic option for the treatment of CD133+ liver-CSC-driven HCC. © 2015 The Authors.-
dc.languageeng-
dc.publisherElsevier (Cell Press): OAJ.-
dc.relation.ispartofStem Cell Reports-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleANXA3/JNK Signaling Promotes Self-Renewal and Tumor Growth, and Its Blockade Provides a Therapeutic Target for Hepatocellular Carcinoma-
dc.typeArticle-
dc.identifier.emailTong, M: caroltm@hku.hk-
dc.identifier.emailFung, TM: ktmfung@hku.hk-
dc.identifier.emailNg, KY: jkyng@hku.hk-
dc.identifier.emailLee, KW: tkwlee@hkucc.hku.hk-
dc.identifier.emailLin, C: nicklin@hku.hk-
dc.identifier.emailYam, JWP: judyyam@pathology.hku.hk-
dc.identifier.emailChan, KW: hrmtckw@hkucc.hku.hk-
dc.identifier.emailNg, F: fng@hku.hk-
dc.identifier.emailZheng, B: bzheng@hkucc.hku.hk-
dc.identifier.emailLo, CM: chungmlo@hkucc.hku.hk-
dc.identifier.emailMan, K: kwanman@hku.hk-
dc.identifier.emailGuan, X: xyguan@hkucc.hku.hk-
dc.identifier.emailMa, SKY: stefma@hku.hk-
dc.identifier.authorityLee, KW=rp00447-
dc.identifier.authorityYam, JWP=rp00468-
dc.identifier.authorityChan, KW=rp00330-
dc.identifier.authorityZheng, B=rp00353-
dc.identifier.authorityLo, CM=rp00412-
dc.identifier.authorityMan, K=rp00417-
dc.identifier.authorityGuan, X=rp00454-
dc.identifier.authorityMa, SKY=rp00506-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1016/j.stemcr.2015.05.013-
dc.identifier.pmid26095609-
dc.identifier.scopuseid_2-s2.0-84937514428-
dc.identifier.hkuros244771-
dc.identifier.volume5-
dc.identifier.issue1-
dc.identifier.spage45-
dc.identifier.epage59-
dc.identifier.isiWOS:000359427500005-
dc.publisher.placeUnited States-

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