MiR-193b promotes autophagy and non-apoptotic cell death in oesophageal cancer cells

Show simple item record

dc.contributor.author Nyhan, Michelle J.
dc.contributor.author O'Donovan, Tracey R.
dc.contributor.author Boersma, Antonius W. M.
dc.contributor.author Wiemer, Erik A. C.
dc.contributor.author McKenna, Sharon L.
dc.date.accessioned 2017-02-24T09:40:15Z
dc.date.available 2017-02-24T09:40:15Z
dc.date.issued 2016-02-15
dc.identifier.citation Nyhan, M. J., O’Donovan, T. R., Boersma, A. W. M., Wiemer, E. A. C. and McKenna, S. L. (2016) 'MiR-193b promotes autophagy and non-apoptotic cell death in oesophageal cancer cells', BMC Cancer, 16(1), pp. 101. doi:10.1186/s12885-016-2123-6 en
dc.identifier.volume 16 en
dc.identifier.startpage 101-1 en
dc.identifier.endpage 101-16 en
dc.identifier.issn 1471-2407
dc.identifier.uri http://hdl.handle.net/10468/3686
dc.identifier.doi 10.1186/s12885-016-2123-6
dc.description.abstract Background: Successful treatment of oesophageal cancer is hampered by recurrent drug resistant disease. We have previously demonstrated the importance of apoptosis and autophagy for the recovery of oesophageal cancer cells following drug treatment. When apoptosis (with autophagy) is induced, these cells are chemosensitive and will not recover following chemotherapy treatment. In contrast, when cancer cells exhibit only autophagy and limited Type II cell death, they are chemoresistant and recover following drug withdrawal. Methods: MicroRNA (miRNA) expression profiling of an oesophageal cancer cell line panel was used to identify miRNAs that were important in the regulation of apoptosis and autophagy. The effects of miRNA overexpression on cell death mechanisms and recovery were assessed in the chemoresistant (autophagy inducing) KYSE450 oesophageal cancer cells. Results: MiR-193b was the most differentially expressed miRNA between the chemosensitive and chemoresistant cell lines with higher expression in chemosensitive apoptosis inducing cell lines. Colony formation assays showed that overexpression of miR-193b significantly impedes the ability of KYSE450 cells to recover following 5-fluorouracil (5-FU) treatment. The critical mRNA targets of miR-193b are unknown but target prediction and siRNA data analysis suggest that it may mediate some of its effects through stathmin 1 regulation. Apoptosis was not involved in the enhanced cytotoxicity. Overexpression of miR-193b in these cells induced autophagic flux and non-apoptotic cell death. Conclusion: These results highlight the importance of miR-193b in determining oesophageal cancer cell viability and demonstrate an enhancement of chemotoxicity that is independent of apoptosis induction. en
dc.description.sponsorship Irish Cancer Society fellowship programme (CRF12NYH); Breakthrough Cancer Research, Cork, Ireland. en
dc.format.mimetype application/pdf en
dc.language.iso en en
dc.publisher BioMed Central en
dc.rights © 2016 Nyhan et al. Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. en
dc.rights.uri http://creativecommons.org/licenses/by/4.0/ en
dc.subject MiR-193b Autophagy en
dc.subject Chemosensitivity en
dc.subject Stathmin 1 en
dc.subject Oesophageal cancer en
dc.subject Non-apoptotic cell death en
dc.title MiR-193b promotes autophagy and non-apoptotic cell death in oesophageal cancer cells en
dc.type Article (peer-reviewed) en
dc.internal.authorcontactother Sharon Mckenna, Surgery, University College Cork, Cork, Ireland. +353-21-490-3000 Email: s.mckenna@ucc.ie en
dc.internal.availability Full text available en
dc.date.updated 2017-02-24T09:32:56Z
dc.description.version Published Version en
dc.internal.rssid 384818086
dc.internal.wokid WOS:000370014400003
dc.contributor.funder Irish Cancer Society en
dc.contributor.funder Breakthrough Cancer Research, Ireland en
dc.description.status Peer reviewed en
dc.identifier.journaltitle BMC Cancer en
dc.internal.copyrightchecked No !!CORA!! en
dc.internal.licenseacceptance Yes en
dc.internal.IRISemailaddress s.mckenna@ucc.ie en


Files in this item

This item appears in the following Collection(s)

Show simple item record

© 2016 Nyhan et al. Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. Except where otherwise noted, this item's license is described as © 2016 Nyhan et al. Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
This website uses cookies. By using this website, you consent to the use of cookies in accordance with the UCC Privacy and Cookies Statement. For more information about cookies and how you can disable them, visit our Privacy and Cookies statement