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Article: MiR-23a-mediated inhibition of topoisomerase 1 expression potentiates cell response to etoposide in human hepatocellular carcinoma

TitleMiR-23a-mediated inhibition of topoisomerase 1 expression potentiates cell response to etoposide in human hepatocellular carcinoma
Authors
Issue Date2013
PublisherBioMed Central Ltd. The Journal's web site is located at http://www.molecular-cancer.com
Citation
Molecular Cancer, 2013, v. 12 n. 1, p. 119 How to Cite?
AbstractBackground: microRNAs have been shown to regulate the chemosensitivity of cancer cells. The aim of this study is to investigate the role and mechanism of mir-23a in enhancing the anti-tumor effect of topoisomerase 2A (TOP2A) poison etoposide in human hepatocellular carcinoma (HCC). Methods: The anti-tumor effect of chemotherapeutic agents in HCC cells were examined in vitro and in vivo xenograft model. Expression of mRNA and miRNAs were determined by quantitative real-time PCR. Protein expression was analyzed by immunoblotting. Results: Overexpression of mir-23a could significantly potentiate the in vitro and in vivo anti-tumor effect of etoposide; however, ectopic expression of miR-23a fails to sensitize HCC cells to 5-fluorouracil treatment, indicating the miR-23a-induced cancer cell hypersensitivity in chemotherapy is TOP2A-specific though miR-23a overexpression could not directly up-regulate TOP2A expression. Topoisomerase 1(TOP1) is down-regulated in miR-23a-overexpressed HCC cells. MiR-23a could directly bind to 3′untranslated region of TOP1 mRNA, and suppress the corresponding protein expression and inhibition of miR-23a further arguments the expression of TOP1. MiR-23a was up-regulated during DNA damage in cancer cells in line with the p53 expression. Up-regulation of p53 induces mir-23a expression, while suppression of p53 inhibits miR-23a in HCC cells. Conclusion: Our study sheds light on the role of miR-23a as a potential target in regulating chemosensitivity of HCC cells. © 2013 Wang et al.; licensee BioMed Central Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/195910
ISSN
2015 Impact Factor: 5.888
2015 SCImago Journal Rankings: 2.337
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWang, Nen_US
dc.contributor.authorZhu, Men_US
dc.contributor.authorTsao, GSWen_US
dc.contributor.authorMan, Ken_US
dc.contributor.authorZhang, Zen_US
dc.contributor.authorFeng, Yen_US
dc.date.accessioned2014-03-21T02:18:27Z-
dc.date.available2014-03-21T02:18:27Z-
dc.date.issued2013en_US
dc.identifier.citationMolecular Cancer, 2013, v. 12 n. 1, p. 119en_US
dc.identifier.issn1476-4598en_US
dc.identifier.urihttp://hdl.handle.net/10722/195910-
dc.description.abstractBackground: microRNAs have been shown to regulate the chemosensitivity of cancer cells. The aim of this study is to investigate the role and mechanism of mir-23a in enhancing the anti-tumor effect of topoisomerase 2A (TOP2A) poison etoposide in human hepatocellular carcinoma (HCC). Methods: The anti-tumor effect of chemotherapeutic agents in HCC cells were examined in vitro and in vivo xenograft model. Expression of mRNA and miRNAs were determined by quantitative real-time PCR. Protein expression was analyzed by immunoblotting. Results: Overexpression of mir-23a could significantly potentiate the in vitro and in vivo anti-tumor effect of etoposide; however, ectopic expression of miR-23a fails to sensitize HCC cells to 5-fluorouracil treatment, indicating the miR-23a-induced cancer cell hypersensitivity in chemotherapy is TOP2A-specific though miR-23a overexpression could not directly up-regulate TOP2A expression. Topoisomerase 1(TOP1) is down-regulated in miR-23a-overexpressed HCC cells. MiR-23a could directly bind to 3′untranslated region of TOP1 mRNA, and suppress the corresponding protein expression and inhibition of miR-23a further arguments the expression of TOP1. MiR-23a was up-regulated during DNA damage in cancer cells in line with the p53 expression. Up-regulation of p53 induces mir-23a expression, while suppression of p53 inhibits miR-23a in HCC cells. Conclusion: Our study sheds light on the role of miR-23a as a potential target in regulating chemosensitivity of HCC cells. © 2013 Wang et al.; licensee BioMed Central Ltd.-
dc.languageengen_US
dc.publisherBioMed Central Ltd. The Journal's web site is located at http://www.molecular-cancer.comen_US
dc.relation.ispartofMolecular Canceren_US
dc.rightsMolecular Cancer. Copyright © BioMed Central Ltd.en_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleMiR-23a-mediated inhibition of topoisomerase 1 expression potentiates cell response to etoposide in human hepatocellular carcinomaen_US
dc.typeArticleen_US
dc.identifier.emailWang, N: ckwang@hku.hken_US
dc.identifier.emailZhu, M: mfzhu@hku.hken_US
dc.identifier.emailTsao, GSW: gswtsao@hku.hken_US
dc.identifier.emailMan, K: kwanman@hku.hken_US
dc.identifier.emailZhang, Z: zhangzj@hkucc.hku.hken_US
dc.identifier.emailFeng, Y: yfeng@hku.hken_US
dc.identifier.authorityTsao, GSW=rp00399en_US
dc.identifier.authorityMan, K=rp00417en_US
dc.identifier.authorityZhang, Z=rp01297en_US
dc.identifier.authorityFeng, Y=rp00466en_US
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1186/1476-4598-12-119en_US
dc.identifier.pmid24103454-
dc.identifier.pmcidPMC3856574-
dc.identifier.scopuseid_2-s2.0-84885000772-
dc.identifier.hkuros228307en_US
dc.identifier.hkuros226724-
dc.identifier.volume12en_US
dc.identifier.issue1en_US
dc.identifier.spage119en_US
dc.identifier.epage119en_US
dc.identifier.isiWOS:000326288400002-
dc.publisher.placeUnited Kingdomen_US

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