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Article: Berberine-induced tumor suppressor p53 up-regulation gets involved in the regulatory network of MIR-23a in hepatocellular carcinoma

TitleBerberine-induced tumor suppressor p53 up-regulation gets involved in the regulatory network of MIR-23a in hepatocellular carcinoma
Authors
Issue Date2014
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/713381/description?navopenmenu=-2
Citation
Biochimica et Biophysica Acta: Gene Regulatory Mechanisms, 2014, v. 1839 n. 9, p. 849-857 How to Cite?
AbstractAim of the study: To investigate the involvement of p53 in the regulatory network of microRNA-23a (miR-23a) in berberine-treated hepatocellular carcinoma (HCC) cells. Methods: The biogenesis of miR-23a upon berberine treatment was monitored by detecting the transcript expression of primary precursor, precursor and mature forms of miR-23a. Protein expression was detected with immunoblotting. The binding capacity between p53 and chromatin DNA was determined by chromatin immunoprecipitation. The role of miR-23a in mediating suppression of HCC by berberine was determined both in vitro and in vivo. Results: miR-23a was up-regulated upon berberine treatment in human HCC cells, and berberine could increase the expression of primary precursor, precursor and mature forms of miR-23a. The up-regulation of miR-23a by berberine is p53-dependent. Inhibition of p53 expression and activity could block the up-regulation of miR-23a induced by berberine. Furthermore, berberine-induced miR-23a expression may mediate the transcription activation of p53-related tumor suppressive genes p21 and GADD45α. Inhibition of miR-23a abolishes the binding of p53 onto chromatin and attenuates transcription activation of p21 and GADD45α. Target prediction and experimental validation demonstrate that berberine-induced miR-23a may target to Nek6 to suppress its expression. Berberine-induced G2/M cell cycle arrest in HCC was attenuated when miR-23a was inhibited. Berberine-induced cell death and in vivo tumor growth inhibition are attenuated upon inhibition of miR-23a. Conclusion: Our study reveals that miR-23a may be involved in regulating the anti-HCC effect of berberine by mediating the regulation of p53. © 2014 Elsevier B.V.
Persistent Identifierhttp://hdl.handle.net/10722/198455
ISSN
2015 Impact Factor: 5.373
2015 SCImago Journal Rankings: 4.460
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWang, N-
dc.contributor.authorZHU, M-
dc.contributor.authorWang, X-
dc.contributor.authorTAN, HY-
dc.contributor.authorTsao, GSW-
dc.contributor.authorFeng, Y-
dc.date.accessioned2014-07-07T06:58:44Z-
dc.date.available2014-07-07T06:58:44Z-
dc.date.issued2014-
dc.identifier.citationBiochimica et Biophysica Acta: Gene Regulatory Mechanisms, 2014, v. 1839 n. 9, p. 849-857-
dc.identifier.issn1874-9399-
dc.identifier.urihttp://hdl.handle.net/10722/198455-
dc.description.abstractAim of the study: To investigate the involvement of p53 in the regulatory network of microRNA-23a (miR-23a) in berberine-treated hepatocellular carcinoma (HCC) cells. Methods: The biogenesis of miR-23a upon berberine treatment was monitored by detecting the transcript expression of primary precursor, precursor and mature forms of miR-23a. Protein expression was detected with immunoblotting. The binding capacity between p53 and chromatin DNA was determined by chromatin immunoprecipitation. The role of miR-23a in mediating suppression of HCC by berberine was determined both in vitro and in vivo. Results: miR-23a was up-regulated upon berberine treatment in human HCC cells, and berberine could increase the expression of primary precursor, precursor and mature forms of miR-23a. The up-regulation of miR-23a by berberine is p53-dependent. Inhibition of p53 expression and activity could block the up-regulation of miR-23a induced by berberine. Furthermore, berberine-induced miR-23a expression may mediate the transcription activation of p53-related tumor suppressive genes p21 and GADD45α. Inhibition of miR-23a abolishes the binding of p53 onto chromatin and attenuates transcription activation of p21 and GADD45α. Target prediction and experimental validation demonstrate that berberine-induced miR-23a may target to Nek6 to suppress its expression. Berberine-induced G2/M cell cycle arrest in HCC was attenuated when miR-23a was inhibited. Berberine-induced cell death and in vivo tumor growth inhibition are attenuated upon inhibition of miR-23a. Conclusion: Our study reveals that miR-23a may be involved in regulating the anti-HCC effect of berberine by mediating the regulation of p53. © 2014 Elsevier B.V.-
dc.languageeng-
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/713381/description?navopenmenu=-2-
dc.relation.ispartofBiochimica et Biophysica Acta: Gene Regulatory Mechanisms-
dc.rights© <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.titleBerberine-induced tumor suppressor p53 up-regulation gets involved in the regulatory network of MIR-23a in hepatocellular carcinoma-
dc.typeArticle-
dc.identifier.emailWang, N: ckwang@hku.hk-
dc.identifier.emailWang, X: xbwang@hku.hk-
dc.identifier.emailTsao, GSW: gswtsao@hku.hk-
dc.identifier.emailFeng, Y: yfeng@hku.hk-
dc.identifier.authorityWang, N=rp02075-
dc.identifier.authorityTsao, GSW=rp00399-
dc.identifier.authorityFeng, Y=rp00466-
dc.identifier.doi10.1016/j.bbagrm.2014.05.027-
dc.identifier.pmid24942805-
dc.identifier.scopuseid_2-s2.0-84904431496-
dc.identifier.hkuros229749-
dc.identifier.volume1839-
dc.identifier.issue9-
dc.identifier.spage849-
dc.identifier.epage857-
dc.identifier.isiWOS:000341347900011-
dc.publisher.placeNetherlands-

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