File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Dietary compound Isoliquiritigenin prevents mammary carcinogenesis by inhibiting breast cancer stem cells through WIF1 demethylation

TitleDietary compound Isoliquiritigenin prevents mammary carcinogenesis by inhibiting breast cancer stem cells through WIF1 demethylation
Authors
Issue Date2015
PublisherImpact Journals LLC. The Journal's web site is located at http://www.impactjournals.com/oncotarget/index.html
Citation
Oncotarget, 2015, v. 6 n. 12, p. 9854-9876 How to Cite?
AbstractBreast cancer stem cells (CSCs) are considered as the root of mammary tumorigenesis. Previous studies have demonstrated that ISL efficiently limited the activities of breast CSCs. However, the cancer prevention activities of ISL and its precise molecular mechanisms remain largely unknown. Here, we report a novel function of ISL as a natural demethylation agent targeting WIF1 to prevent breast cancer. ISL administration suppressed in vivo breast cancer initiation and progression, accompanied by reduced CSC-like populations. A global gene expression profile assay further identified WIF1 as the main response gene of ISL treatment, accompanied by the simultaneous downregulation of β-catenin signaling and G0/G1 phase arrest in breast CSCs. In addition, WIF1 inhibition significantly relieved the CSC-limiting effects of ISL and methylation analysis further revealed that ISL enhanced WIF1 gene expression via promoting the demethylation of its promoter, which was closely correlated with the inhibition of DNMT1 methyltransferase. Molecular docking analysis finally revealed that ISL could stably dock into the catalytic domain of DNMT1. Taken together, our findings not only provide preclinical evidence to demonstrate the use of ISL as a dietary supplement to inhibit mammary carcinogenesis but also shed novel light on WIF1 as an epigenetic target for breast cancer prevention.
Persistent Identifierhttp://hdl.handle.net/10722/216797
ISSN
2015 Impact Factor: 5.008
2015 SCImago Journal Rankings: 2.294
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWang, N-
dc.contributor.authorWang, Z-
dc.contributor.authorWang, Y-
dc.contributor.authorShen, J-
dc.contributor.authorPeng, C-
dc.contributor.authorYOU, J-
dc.contributor.authorPENG, F-
dc.contributor.authorGuan, X-
dc.contributor.authorChen, J-
dc.date.accessioned2015-09-18T05:38:45Z-
dc.date.available2015-09-18T05:38:45Z-
dc.date.issued2015-
dc.identifier.citationOncotarget, 2015, v. 6 n. 12, p. 9854-9876-
dc.identifier.issn1949-2553-
dc.identifier.urihttp://hdl.handle.net/10722/216797-
dc.description.abstractBreast cancer stem cells (CSCs) are considered as the root of mammary tumorigenesis. Previous studies have demonstrated that ISL efficiently limited the activities of breast CSCs. However, the cancer prevention activities of ISL and its precise molecular mechanisms remain largely unknown. Here, we report a novel function of ISL as a natural demethylation agent targeting WIF1 to prevent breast cancer. ISL administration suppressed in vivo breast cancer initiation and progression, accompanied by reduced CSC-like populations. A global gene expression profile assay further identified WIF1 as the main response gene of ISL treatment, accompanied by the simultaneous downregulation of β-catenin signaling and G0/G1 phase arrest in breast CSCs. In addition, WIF1 inhibition significantly relieved the CSC-limiting effects of ISL and methylation analysis further revealed that ISL enhanced WIF1 gene expression via promoting the demethylation of its promoter, which was closely correlated with the inhibition of DNMT1 methyltransferase. Molecular docking analysis finally revealed that ISL could stably dock into the catalytic domain of DNMT1. Taken together, our findings not only provide preclinical evidence to demonstrate the use of ISL as a dietary supplement to inhibit mammary carcinogenesis but also shed novel light on WIF1 as an epigenetic target for breast cancer prevention.-
dc.languageeng-
dc.publisherImpact Journals LLC. The Journal's web site is located at http://www.impactjournals.com/oncotarget/index.html-
dc.relation.ispartofOncotarget-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleDietary compound Isoliquiritigenin prevents mammary carcinogenesis by inhibiting breast cancer stem cells through WIF1 demethylation-
dc.typeArticle-
dc.identifier.emailWang, Y: yuwanghk@hku.hk-
dc.identifier.emailShen, J: shenjg@hku.hk-
dc.identifier.emailGuan, X: xyguan@hkucc.hku.hk-
dc.identifier.emailChen, J: abchen@hkucc.hku.hk-
dc.identifier.authorityWang, Y=rp00239-
dc.identifier.authorityShen, J=rp00487-
dc.identifier.authorityGuan, X=rp00454-
dc.identifier.authorityChen, J=rp01316-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.18632/oncotarget.3396-
dc.identifier.pmid25918249-
dc.identifier.pmcidPMC4496402-
dc.identifier.scopuseid_2-s2.0-84929590467-
dc.identifier.hkuros250624-
dc.identifier.volume6-
dc.identifier.issue12-
dc.identifier.spage9854-
dc.identifier.epage9876-
dc.identifier.isiWOS:000358874600019-
dc.publisher.placeUnited States-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats