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Conference Paper: miR-29c modulates chemoresistance in esophageal cancer cells by suppressing FBXO31

TitlemiR-29c modulates chemoresistance in esophageal cancer cells by suppressing FBXO31
Authors
Issue Date2016
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/ejca
Citation
The 24th Biennial Congress of the European Association for Cancer Research (EACR-24), Manchester, UK., 9-12 July 2016. In European Journal of Cancer, 2016, v. 61 suppl. 1, p. S64, abstract no. 326 How to Cite?
AbstractBACKGROUND: Esophageal cancer is the 6th most common cause of cancer-related death worldwide. Multimodal treatment combining surgical resection and the use of chemotherapeutic drugs is commonly used in the management of this disease. However, resistance to chemotherapy drugs may contribute to poor treatment outcome. A better understanding of the molecular mechanisms of chemoresistance will facilitate the development of novel therapies. MATERIAL AND METHODS: Esophageal squamous cell carcinoma (ESCC) cell line models of acquired chemoresistance to 5-fluorouracil (5-FU) were established by exposing ESCC cell lines to increasing concentrations of 5-FU for over 18 months. These 5-FU-resistance (FR) sublines were used to identify microRNAs (miRNAs) and genes associated with 5-FU resistance using an integrative approach that combined Taqman miRNA array, cDNA microarray and in silico analysis. RESULTS AND DISCUSSION: Microarray analysis of miRNA expression in FR and parental cells showed that miR-29c was one of the most downregulated miRNAs in the FR sublines. cDNA microarray data showed that FBXO31, a predicted target of miR-29c, was amongst the upregulated mRNAs in the FR cells. We found that overexpression of miR-29c could restore 5-FU chemosensitivity in FR cells and suppress FBXO31 protein expression in ESCC cell lines. Re-expression of FBXO31 in miR-29c-overexpressing ESCC cells abrogated the effects of miR-29c on 5-FU chemosensitivity. Moreover, FBXO31 overexpression enhanced, whereas FBXO31-knockdown reduced, the sensitivity of ESCC cells to cisplatin both in vitro and in vivo. CONCLUSION: Our data suggest that miR-29c can modulate the chemosensitivity of ESCC cells by regulating FBXO31. Since FBXO31 has prognostic significance in patients with ESCC, this miR-29c/FBXO31 regulatory mechanism may be exploited to develop novel biomarkers and therapeutic strategies to improve patient survival.
DescriptionThis journal suppl. entitled: 24th Biennial Congress of the European Association for Cancer Research, 9–12 July 2016, Manchester, UK
Persistent Identifierhttp://hdl.handle.net/10722/229940
ISSN
2015 Impact Factor: 6.163
2015 SCImago Journal Rankings: 3.152

 

DC FieldValueLanguage
dc.contributor.authorCheung, A-
dc.contributor.authorLi, B-
dc.contributor.authorXu, W-
dc.contributor.authorLiu, J-
dc.contributor.authorChan, KW-
dc.date.accessioned2016-08-23T14:14:13Z-
dc.date.available2016-08-23T14:14:13Z-
dc.date.issued2016-
dc.identifier.citationThe 24th Biennial Congress of the European Association for Cancer Research (EACR-24), Manchester, UK., 9-12 July 2016. In European Journal of Cancer, 2016, v. 61 suppl. 1, p. S64, abstract no. 326-
dc.identifier.issn0959-8049-
dc.identifier.urihttp://hdl.handle.net/10722/229940-
dc.descriptionThis journal suppl. entitled: 24th Biennial Congress of the European Association for Cancer Research, 9–12 July 2016, Manchester, UK-
dc.description.abstractBACKGROUND: Esophageal cancer is the 6th most common cause of cancer-related death worldwide. Multimodal treatment combining surgical resection and the use of chemotherapeutic drugs is commonly used in the management of this disease. However, resistance to chemotherapy drugs may contribute to poor treatment outcome. A better understanding of the molecular mechanisms of chemoresistance will facilitate the development of novel therapies. MATERIAL AND METHODS: Esophageal squamous cell carcinoma (ESCC) cell line models of acquired chemoresistance to 5-fluorouracil (5-FU) were established by exposing ESCC cell lines to increasing concentrations of 5-FU for over 18 months. These 5-FU-resistance (FR) sublines were used to identify microRNAs (miRNAs) and genes associated with 5-FU resistance using an integrative approach that combined Taqman miRNA array, cDNA microarray and in silico analysis. RESULTS AND DISCUSSION: Microarray analysis of miRNA expression in FR and parental cells showed that miR-29c was one of the most downregulated miRNAs in the FR sublines. cDNA microarray data showed that FBXO31, a predicted target of miR-29c, was amongst the upregulated mRNAs in the FR cells. We found that overexpression of miR-29c could restore 5-FU chemosensitivity in FR cells and suppress FBXO31 protein expression in ESCC cell lines. Re-expression of FBXO31 in miR-29c-overexpressing ESCC cells abrogated the effects of miR-29c on 5-FU chemosensitivity. Moreover, FBXO31 overexpression enhanced, whereas FBXO31-knockdown reduced, the sensitivity of ESCC cells to cisplatin both in vitro and in vivo. CONCLUSION: Our data suggest that miR-29c can modulate the chemosensitivity of ESCC cells by regulating FBXO31. Since FBXO31 has prognostic significance in patients with ESCC, this miR-29c/FBXO31 regulatory mechanism may be exploited to develop novel biomarkers and therapeutic strategies to improve patient survival.-
dc.languageeng-
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/ejca-
dc.relation.ispartofEuropean Journal of Cancer-
dc.rightsPosting accepted manuscript (postprint): © <year>. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/-
dc.titlemiR-29c modulates chemoresistance in esophageal cancer cells by suppressing FBXO31-
dc.typeConference_Paper-
dc.identifier.emailCheung, A: lmcheung@hku.hk-
dc.identifier.emailLi, B: libinhku@hkucc.hku.hk-
dc.identifier.emailXu, W: wenwenxu@hku.hk-
dc.identifier.emailLiu, J: liuj614@hku.hk-
dc.identifier.emailChan, KW: kwchan@pathology.hku.hk-
dc.identifier.authorityCheung, A=rp00332-
dc.identifier.authorityChan, KW=rp00330-
dc.identifier.doi10.1016/S0959-8049(16)61222-4-
dc.identifier.hkuros262176-
dc.identifier.volume61-
dc.identifier.issuesuppl. 1-
dc.identifier.spageS64, abstract no. 326-
dc.identifier.epageS64, abstract no. 326-
dc.publisher.placeUnited Kingdom-

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