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Conference Paper: Identification of miR-29c/FBXO31 as a key regulatory mechanism in esophageal cancer chemoresistance

TitleIdentification of miR-29c/FBXO31 as a key regulatory mechanism in esophageal cancer chemoresistance
Authors
Issue Date2015
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/CHE
Citation
The 2015 International Conference on Antimicrobial Agents and Chemotherapy, Valencia, Spain, 4-6 August 2015. In Chemotherapy, 2015, v. 4 n. 2, p. 56 How to Cite?
AbstractEsophageal cancer ranks as the 6th most frequent cause of cancer death in the world. Chemoresistance is a major obstacle in cancer therapy, but the mechanism remains unclear. MicroRNAs have received increasing attention as a novel and promising targets in cancer diagnosis, prognosis and treatment. Identification and experimental validation of the chemoresistance-related miRNAs in esophageal cancer are urgently needed. We have established esophageal squamous cell carcinoma (ESCC) cell line models of acquired chemoresistance to 5-FU (FR sublines). MicroRNA profiling and subsequent RT-PCR confirmation showed that miR-29c was one of the most down-regulated miRNA in FR sublines. We found that miR-29c overexpression could revert acquired chemoresistance of FR cells, and that lower miR-29c expression in ESCC was associated with poor survival of patients. FBXO31, a novel F Box protein with prognostic significance in ESCC, was amongst the upregulated mRNAs identified in the FR cells using cDNA microarray and was predicted by comtputational algorithms to be a target of miR-29c. Our data showed that FBXO31 increased chemoresistance of ESCC cells in vitro and in vivo, and that ectopic expression of miR-29c significantly reduced FBXO31 expression. More importantly, FBXO31 mediated the functions of miR-29c in chemoresistance of ESCC cells. In summary, this study greatly enhances our understanding of the functions of miR-29c and FBXO31 in esophageal cancer; their significance in diagnosis, prognosis and treatment warrants further investigation.
DescriptionOpen Access Journal
Persistent Identifierhttp://hdl.handle.net/10722/214999
ISSN
2015 Impact Factor: 0.992
2015 SCImago Journal Rankings: 0.630

 

DC FieldValueLanguage
dc.contributor.authorLi, B-
dc.contributor.authorXu, W-
dc.contributor.authorLiu, J-
dc.contributor.authorCheung, ALM-
dc.date.accessioned2015-08-21T12:17:52Z-
dc.date.available2015-08-21T12:17:52Z-
dc.date.issued2015-
dc.identifier.citationThe 2015 International Conference on Antimicrobial Agents and Chemotherapy, Valencia, Spain, 4-6 August 2015. In Chemotherapy, 2015, v. 4 n. 2, p. 56-
dc.identifier.issn0009-3157-
dc.identifier.urihttp://hdl.handle.net/10722/214999-
dc.descriptionOpen Access Journal-
dc.description.abstractEsophageal cancer ranks as the 6th most frequent cause of cancer death in the world. Chemoresistance is a major obstacle in cancer therapy, but the mechanism remains unclear. MicroRNAs have received increasing attention as a novel and promising targets in cancer diagnosis, prognosis and treatment. Identification and experimental validation of the chemoresistance-related miRNAs in esophageal cancer are urgently needed. We have established esophageal squamous cell carcinoma (ESCC) cell line models of acquired chemoresistance to 5-FU (FR sublines). MicroRNA profiling and subsequent RT-PCR confirmation showed that miR-29c was one of the most down-regulated miRNA in FR sublines. We found that miR-29c overexpression could revert acquired chemoresistance of FR cells, and that lower miR-29c expression in ESCC was associated with poor survival of patients. FBXO31, a novel F Box protein with prognostic significance in ESCC, was amongst the upregulated mRNAs identified in the FR cells using cDNA microarray and was predicted by comtputational algorithms to be a target of miR-29c. Our data showed that FBXO31 increased chemoresistance of ESCC cells in vitro and in vivo, and that ectopic expression of miR-29c significantly reduced FBXO31 expression. More importantly, FBXO31 mediated the functions of miR-29c in chemoresistance of ESCC cells. In summary, this study greatly enhances our understanding of the functions of miR-29c and FBXO31 in esophageal cancer; their significance in diagnosis, prognosis and treatment warrants further investigation.-
dc.languageeng-
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/CHE-
dc.relation.ispartofChemotherapy-
dc.rightsChemotherapy. Copyright © S Karger AG.-
dc.titleIdentification of miR-29c/FBXO31 as a key regulatory mechanism in esophageal cancer chemoresistance-
dc.typeConference_Paper-
dc.identifier.emailLi, B: libinhku@hkucc.hku.hk-
dc.identifier.emailCheung, ALM: lmcheung@hku.hk-
dc.identifier.authorityCheung, ALM=rp00332-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.4172/2167-7700.S1.002-
dc.identifier.hkuros250001-
dc.identifier.volume4-
dc.identifier.issue2-
dc.identifier.spage56-
dc.identifier.epage56-
dc.publisher.placeSwitzerland-

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