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Conference Paper: Estradiol activated microrna 23a directly or synergistically with p53 implicated in sex difference in hepatocellular carcinoma development

TitleEstradiol activated microrna 23a directly or synergistically with p53 implicated in sex difference in hepatocellular carcinoma development
Authors
KeywordsMedical sciences
Endocrinology
Issue Date2015
PublisherSpringer New York LLC. The Journal's web site is located at http://www.springer.com/west/home/medicine?SGWID=4-10054-70-173733513-0
Citation
The 24th Annual Conference of the Asian Pacific Association for the Study of the Liver (APASL 2015), Istanbul, Turkey, 12-15 March 2015. In Hepatology International, 2015, v. 9 suppl. 1, p. S137, abstract no. 2102-S138 How to Cite?
AbstractBACKGROUND: Estrogen (E2) exerts a protective role against hepatocellular carcinoma (HCC) development. We sought to determine the effects of E2 on apoptotic miRNAs expression and explore the possible mechanism underlying apoptosis in HCC. METHODS: Microarray was performed to analyze alteration of apoptotic miRNAs in E2-treated liver cell-line. Expression profiles of selected miRNAs were verified using qRT-PCR. qRT-PCR and Western-blot were used to analyze the alteration of mRNA and protein levels of genes such as p53, ERa, XIAP and caspase-3/7. Activity of caspase3/7 was measured using a luminescent assay. RESULTS: After E2 treatment, more than twofold alteration was observed in 25 upregulated and 10 downregulated miRNAs. Expression of miR-23a in p53-mutated male cell-lines was significantly lower than cell-lines with functional p53 (all P\0.001), but not in female cells. p53 activation increased miR-23a expression in p53 +/+ HepG2 cells (P\0.0001 at 12 h. P\0.01 at 24 h), but not in p53-/-Hep3B cells. E2 via ERa could significantly activated miR- 23a (P\0.001) and p53 (P\0.01) expression, and thus replenished p53-deficiency SNU387 cells in activation of miR-23a. Moreover, miR-23a mimic and E2 significantly activated miR-23a (P\0.001) and suppressed the expression of its target XIAP (P\0.0001 and P\0.01). Decreasing of XIAP contributes to activation of caspase-3 activity and cell apoptosis. Caspase-3 mRNA was significantly upregulated with E2 and miR-23a mimic treatment (P\0.0001 for E2, and P\0.01 for miR-23a mimic). Treatment of cells with anitmiR- 23a increased XIAP expression (P\0.001), and abolished caspase-3 activation (P\0.001). CONCLUSIONS: This study revealed a novel E2-signaling mechanism in regulating miRNAs expression and apoptosis that may contribute to sex difference in HCC development.
DescriptionConference Theme: New Horizons from East to west in Hepatology
Topic 4: Basic Science of Hepatology: no. 2102
This journal suppl. entitled: Conference Abstracts: 24th Annual Conference of APASL, March 12-15, 2015, Istanbul, Turkey
Persistent Identifierhttp://hdl.handle.net/10722/214127
ISSN
2015 Impact Factor: 1.125
2015 SCImago Journal Rankings: 0.669

 

DC FieldValueLanguage
dc.contributor.authorHuang, FY-
dc.contributor.authorWong, DKH-
dc.contributor.authorSeto, WK-
dc.contributor.authorLai, CL-
dc.contributor.authorYuen, MF-
dc.date.accessioned2015-08-21T03:08:36Z-
dc.date.available2015-08-21T03:08:36Z-
dc.date.issued2015-
dc.identifier.citationThe 24th Annual Conference of the Asian Pacific Association for the Study of the Liver (APASL 2015), Istanbul, Turkey, 12-15 March 2015. In Hepatology International, 2015, v. 9 suppl. 1, p. S137, abstract no. 2102-S138-
dc.identifier.issn1936-0533-
dc.identifier.urihttp://hdl.handle.net/10722/214127-
dc.descriptionConference Theme: New Horizons from East to west in Hepatology-
dc.descriptionTopic 4: Basic Science of Hepatology: no. 2102-
dc.descriptionThis journal suppl. entitled: Conference Abstracts: 24th Annual Conference of APASL, March 12-15, 2015, Istanbul, Turkey-
dc.description.abstractBACKGROUND: Estrogen (E2) exerts a protective role against hepatocellular carcinoma (HCC) development. We sought to determine the effects of E2 on apoptotic miRNAs expression and explore the possible mechanism underlying apoptosis in HCC. METHODS: Microarray was performed to analyze alteration of apoptotic miRNAs in E2-treated liver cell-line. Expression profiles of selected miRNAs were verified using qRT-PCR. qRT-PCR and Western-blot were used to analyze the alteration of mRNA and protein levels of genes such as p53, ERa, XIAP and caspase-3/7. Activity of caspase3/7 was measured using a luminescent assay. RESULTS: After E2 treatment, more than twofold alteration was observed in 25 upregulated and 10 downregulated miRNAs. Expression of miR-23a in p53-mutated male cell-lines was significantly lower than cell-lines with functional p53 (all P\0.001), but not in female cells. p53 activation increased miR-23a expression in p53 +/+ HepG2 cells (P\0.0001 at 12 h. P\0.01 at 24 h), but not in p53-/-Hep3B cells. E2 via ERa could significantly activated miR- 23a (P\0.001) and p53 (P\0.01) expression, and thus replenished p53-deficiency SNU387 cells in activation of miR-23a. Moreover, miR-23a mimic and E2 significantly activated miR-23a (P\0.001) and suppressed the expression of its target XIAP (P\0.0001 and P\0.01). Decreasing of XIAP contributes to activation of caspase-3 activity and cell apoptosis. Caspase-3 mRNA was significantly upregulated with E2 and miR-23a mimic treatment (P\0.0001 for E2, and P\0.01 for miR-23a mimic). Treatment of cells with anitmiR- 23a increased XIAP expression (P\0.001), and abolished caspase-3 activation (P\0.001). CONCLUSIONS: This study revealed a novel E2-signaling mechanism in regulating miRNAs expression and apoptosis that may contribute to sex difference in HCC development.-
dc.languageeng-
dc.publisherSpringer New York LLC. The Journal's web site is located at http://www.springer.com/west/home/medicine?SGWID=4-10054-70-173733513-0-
dc.relation.ispartofHepatology International-
dc.rightsThe final publication is available at Springer via http://dx.doi.org/10.1007/s12072-015-9609-1-
dc.subjectMedical sciences-
dc.subjectEndocrinology-
dc.titleEstradiol activated microrna 23a directly or synergistically with p53 implicated in sex difference in hepatocellular carcinoma development-
dc.typeConference_Paper-
dc.identifier.emailHuang, FY: fungyu@hkucc.hku.hk-
dc.identifier.emailWong, DKH: danywong@hku.hk-
dc.identifier.emailSeto, WK: wkseto@hku.hk-
dc.identifier.emailLai, CL: hrmelcl@hkucc.hku.hk-
dc.identifier.emailYuen, MF: mfyuen@hku.hk-
dc.identifier.authorityWong, DKH=rp00492-
dc.identifier.authoritySeto, WK=rp01659-
dc.identifier.authorityLai, CL=rp00314-
dc.identifier.authorityYuen, MF=rp00479-
dc.identifier.doi10.1007/s12072-015-9609-1-
dc.identifier.hkuros248043-
dc.identifier.volume9-
dc.identifier.issuesuppl. 1-
dc.identifier.spageS137, abstract no. 2102-
dc.identifier.epageS138-
dc.publisher.placeUnited States-

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