<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>10(4)</volume><submitter>Cui H</submitter><pubmed_abstract>The de-regulation of the miR-29 family and DNA methyltransferase 3A (DNMT3A) is associated with gastric cancer (GC). While increasing evidence indicates miR-29b/c could regulate DNA methylation by targeting DNMT3A, it is currently unknown if epigenetic silencing of miR-29b/c via promoter hypermethylation in GC is caused by abnormal expression of DNMT3A. Thus, we aimed to evaluate whether cross-talk regulation exists between miR-29b/c and DNMT3A and whether it is associated with a malignant phenotype in GC. First, wound healing and Transwell assays revealed that miR-29b/c suppresses tumor metastasis in GC. A luciferase reporter assay demonstrated that DNMT3A is a direct target of miR-29b/c. We used bisulfite genomic sequencing to analyze the DNA methylation status of miR-29b/c. The percenta</pubmed_abstract><journal>PloS one</journal><pagination>e0123926</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4398372</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Deregulation between miR-29b/c and DNMT3A is associated with epigenetic silencing of the CDH1 gene, affecting cell migration and invasion in gastric cancer.</pubmed_title><pmcid>PMC4398372</pmcid><pubmed_authors>Fan H</pubmed_authors><pubmed_authors>Zhao C</pubmed_authors><pubmed_authors>Zhang K</pubmed_authors><pubmed_authors>Gong P</pubmed_authors><pubmed_authors>Zhou R</pubmed_authors><pubmed_authors>Cui H</pubmed_authors><pubmed_authors>Zhang S</pubmed_authors><pubmed_authors>Zhao Z</pubmed_authors><pubmed_authors>Wang L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Deregulation between miR-29b/c and DNMT3A is associated with epigenetic silencing of the CDH1 gene, affecting cell migration and invasion in gastric cancer.</name><description>The de-regulation of the miR-29 family and DNA methyltransferase 3A (DNMT3A) is associated with gastric cancer (GC). While increasing evidence indicates miR-29b/c could regulate DNA methylation by targeting DNMT3A, it is currently unknown if epigenetic silencing of miR-29b/c via promoter hypermethylation in GC is caused by abnormal expression of DNMT3A. Thus, we aimed to evaluate whether cross-talk regulation exists between miR-29b/c and DNMT3A and whether it is associated with a malignant phenotype in GC. First, wound healing and Transwell assays revealed that miR-29b/c suppresses tumor metastasis in GC. A luciferase reporter assay demonstrated that DNMT3A is a direct target of miR-29b/c. We used bisulfite genomic sequencing to analyze the DNA methylation status of miR-29b/c. The percenta</description><dates><release>2015-01-01T00:00:00Z</release><publication>2015</publication><modification>2025-04-04T23:23:56.988Z</modification><creation>2019-03-26T23:32:04Z</creation></dates><accession>S-EPMC4398372</accession><cross_references><pubmed>25874772</pubmed><doi>10.1371/journal.pone.0123926</doi></cross_references></HashMap>