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Article: IGF2 induces CD133 expression in esophageal cancer cells to promote cancer stemness

TitleIGF2 induces CD133 expression in esophageal cancer cells to promote cancer stemness
Authors
Issue Date2018
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canlet
Citation
Cancer Letters, 2018, v. 425, p. 88-100 How to Cite?
AbstractFailure to eradicate cancer stem cells (CSC) during primary therapy may lead to cancer recurrence. We recently reported that CD133 is a functional biomarker for CSCs in esophageal squamous cell carcinoma (ESCC) but the molecular pathways critical for maintenance of CD133-positive CSCs are largely unknown. Here, we revealed that knockdown of IGF2 or treatment with PI3K/AKT inhibitors markedly inhibited the abilities of CD133-positive ESCC cells to self-renew, resist chemotherapeutic drugs, and form tumors. Further functional analysis identified miR-377 as a downstream regulator of PI3K/AKT signaling, and a mediator of the effects of IGF2 on CD133 expression and CSC properties. We found that the expression levels of IGF2 and CD133 were positively correlated with each other in primary ESCC, and that concurrent elevation of IGF2 and CD133 expression was significantly associated with poor patient survival. Furthermore, in vivo experiments demonstrated that IGF2-neutralizing antibody enhanced the sensitivity of tumor xenografts in nude mice to 5-fluorouracil treatment. This study underpins the importance of the IGF2-PI3K/AKT-miR-377-CD133 signaling axis in the maintenance of cancer stemness and in the development of novel therapeutic strategy for treatment of esophageal cancer.
Persistent Identifierhttp://hdl.handle.net/10722/252311
ISSN
2017 Impact Factor: 6.491
2015 SCImago Journal Rankings: 2.331
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorXu, WW-
dc.contributor.authorLi, B-
dc.contributor.authorZhao, JF-
dc.contributor.authorYang, JG-
dc.contributor.authorLi, JQ-
dc.contributor.authorTsao, GSW-
dc.contributor.authorHe, QY-
dc.contributor.authorCheung, A-
dc.date.accessioned2018-04-17T06:09:11Z-
dc.date.available2018-04-17T06:09:11Z-
dc.date.issued2018-
dc.identifier.citationCancer Letters, 2018, v. 425, p. 88-100-
dc.identifier.issn0304-3835-
dc.identifier.urihttp://hdl.handle.net/10722/252311-
dc.description.abstractFailure to eradicate cancer stem cells (CSC) during primary therapy may lead to cancer recurrence. We recently reported that CD133 is a functional biomarker for CSCs in esophageal squamous cell carcinoma (ESCC) but the molecular pathways critical for maintenance of CD133-positive CSCs are largely unknown. Here, we revealed that knockdown of IGF2 or treatment with PI3K/AKT inhibitors markedly inhibited the abilities of CD133-positive ESCC cells to self-renew, resist chemotherapeutic drugs, and form tumors. Further functional analysis identified miR-377 as a downstream regulator of PI3K/AKT signaling, and a mediator of the effects of IGF2 on CD133 expression and CSC properties. We found that the expression levels of IGF2 and CD133 were positively correlated with each other in primary ESCC, and that concurrent elevation of IGF2 and CD133 expression was significantly associated with poor patient survival. Furthermore, in vivo experiments demonstrated that IGF2-neutralizing antibody enhanced the sensitivity of tumor xenografts in nude mice to 5-fluorouracil treatment. This study underpins the importance of the IGF2-PI3K/AKT-miR-377-CD133 signaling axis in the maintenance of cancer stemness and in the development of novel therapeutic strategy for treatment of esophageal cancer.-
dc.languageeng-
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canlet-
dc.relation.ispartofCancer Letters-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleIGF2 induces CD133 expression in esophageal cancer cells to promote cancer stemness-
dc.typeArticle-
dc.identifier.emailTsao, GSW: gswtsao@hku.hk-
dc.identifier.emailCheung, A: lmcheung@hku.hk-
dc.identifier.authorityTsao, GSW=rp00399-
dc.identifier.authorityCheung, A=rp00332-
dc.description.naturepostprint-
dc.identifier.doi10.1016/j.canlet.2018.03.039-
dc.identifier.hkuros284875-
dc.identifier.volume425-
dc.identifier.spage88-
dc.identifier.epage100-
dc.identifier.isiWOS:000432760900009-
dc.publisher.placeIreland-

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