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Article: Epigenetic silencing of miR-490-3p reactivates the chromatin remodeler SMARCD1 to promote helicobacter pylori-induced gastric carcinogenesis

TitleEpigenetic silencing of miR-490-3p reactivates the chromatin remodeler SMARCD1 to promote helicobacter pylori-induced gastric carcinogenesis
Authors
Issue Date2015
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
Cancer Research, 2015, v. 75 n. 4, p. 754-765 How to Cite?
AbstractChromatin remodeling has emerged as a hallmark of gastric cancer, but the regulation of chromatin regulators other than genetic change is unknown. Helicobacter pylori causes epigenetic dysregulation to promote gastric carcinogenesis, but the roles and functions of microRNAs (miRNA) in this multistage cascade are not fully explored. In this study, miRNA expression in preneoplastic and neoplastic lesions in murine stomachs induced by H. pylori and N-methyl-N-nitrosourea (MNU) was profiled by miRNA expression array. miR-490-3p exhibited progressive downregulation in gastritis, intestinal metaplasia, and adenocarcinoma during H. pylori and MNU-induced gastric carcinogenesis. Significant downregulation of miR-490-3p was confirmed in human gastric cancer tissues in which its regulatory region was found to be hypermethylated. miR-490-3p exerted growth- and metastasis-suppressive effects on gastric cancer cells through directly targeting SMARCD1, a SWItch/Sucrose NonFermentable (SWI/SNF) chromatin remodeling complex subunit. Knockdown of SMARCD1 significantly attenuated the protumorigenic effects of miR-490-3p inhibitor, whereas enforced expression of SMARCD1 promoted in vitro and in vivo oncogenic phenotypes of gastric cancer cells. SMARCD1 was markedly upregulated in gastric cancer in which its high expression was associated with shortened patients' survival independent of TNM staging. In conclusion, hypermethylation-mediated silencing of miR-490-3p reactivates SMARCD1 to confer malignant phenotypes, mechanistically linking H. pylori, chromatin remodeling, and gastric carcinogenesis. Cancer Res; 75(4); 754–65. ©2014 AACR.
DescriptionBronze open access
Persistent Identifierhttp://hdl.handle.net/10722/301138
ISSN
2023 Impact Factor: 12.5
2023 SCImago Journal Rankings: 3.468
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorShen, J-
dc.contributor.authorXiao, Z-
dc.contributor.authorWu, WKK-
dc.contributor.authorWang, MH-
dc.contributor.authorTo, KF-
dc.contributor.authorChen, Y-
dc.contributor.authorYang, W-
dc.contributor.authorLi, MSM-
dc.contributor.authorShin, VY-
dc.contributor.authorTong, JH-
dc.contributor.authorKang, W-
dc.contributor.authorZhang, L-
dc.contributor.authorLi, M-
dc.contributor.authorWang, L-
dc.contributor.authorLu, L-
dc.contributor.authorChan, RLY-
dc.contributor.authorWong, SH-
dc.contributor.authorYu, J-
dc.contributor.authorChan, MTV-
dc.contributor.authorChan, FKL-
dc.contributor.authorSung, JJY-
dc.contributor.authorCheng, ASL-
dc.contributor.authorCho, CH-
dc.date.accessioned2021-07-27T08:06:41Z-
dc.date.available2021-07-27T08:06:41Z-
dc.date.issued2015-
dc.identifier.citationCancer Research, 2015, v. 75 n. 4, p. 754-765-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/301138-
dc.descriptionBronze open access-
dc.description.abstractChromatin remodeling has emerged as a hallmark of gastric cancer, but the regulation of chromatin regulators other than genetic change is unknown. Helicobacter pylori causes epigenetic dysregulation to promote gastric carcinogenesis, but the roles and functions of microRNAs (miRNA) in this multistage cascade are not fully explored. In this study, miRNA expression in preneoplastic and neoplastic lesions in murine stomachs induced by H. pylori and N-methyl-N-nitrosourea (MNU) was profiled by miRNA expression array. miR-490-3p exhibited progressive downregulation in gastritis, intestinal metaplasia, and adenocarcinoma during H. pylori and MNU-induced gastric carcinogenesis. Significant downregulation of miR-490-3p was confirmed in human gastric cancer tissues in which its regulatory region was found to be hypermethylated. miR-490-3p exerted growth- and metastasis-suppressive effects on gastric cancer cells through directly targeting SMARCD1, a SWItch/Sucrose NonFermentable (SWI/SNF) chromatin remodeling complex subunit. Knockdown of SMARCD1 significantly attenuated the protumorigenic effects of miR-490-3p inhibitor, whereas enforced expression of SMARCD1 promoted in vitro and in vivo oncogenic phenotypes of gastric cancer cells. SMARCD1 was markedly upregulated in gastric cancer in which its high expression was associated with shortened patients' survival independent of TNM staging. In conclusion, hypermethylation-mediated silencing of miR-490-3p reactivates SMARCD1 to confer malignant phenotypes, mechanistically linking H. pylori, chromatin remodeling, and gastric carcinogenesis. Cancer Res; 75(4); 754–65. ©2014 AACR.-
dc.languageeng-
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/-
dc.relation.ispartofCancer Research-
dc.titleEpigenetic silencing of miR-490-3p reactivates the chromatin remodeler SMARCD1 to promote helicobacter pylori-induced gastric carcinogenesis-
dc.typeArticle-
dc.identifier.emailShin, VY: vyshin@hku.hk-
dc.identifier.authorityShin, VY=rp02000-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1158/0008-5472.CAN-14-1301-
dc.identifier.pmid25503559-
dc.identifier.scopuseid_2-s2.0-84923163426-
dc.identifier.hkuros323794-
dc.identifier.volume75-
dc.identifier.issue4-
dc.identifier.spage754-
dc.identifier.epage765-
dc.identifier.isiWOS:000349841600015-
dc.publisher.placeUnited States-

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