<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>13</volume><submitter>Duan Y</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>microRNAs are small noncoding RNAs that modulate a variety of cellular processes by regulating multiple targets, which can promote or inhibit the development of malignant behaviors. Accumulating evidence suggests miR-24 plays important roles in human carcinogenesis. However, its precise biological role remains largely elusive. This study examined the role of miR-24 in gastric cancer (GC).&lt;h4>Methods&lt;/h4>The expression of miR-24 in GC tissues compared with matched non-tumor tissues and GC cells was detected by qRT-PCR. Synthetic short single or double stranded RNA oligonucleotides and lentiviral vectors were used to regulate miR-24 expression in GC cells to investigate its function in vitro and in vivo.&lt;h4>Results&lt;/h4>miR-24 was significantly downregulated in GC tissues compared with matched non-tumor tissues and was associated with tumor differentiation. Ectopic expression of miR-24 in SGC-7901 GC cells suppressed cell proliferation, migration and invasion in vitro as well as tumorigenicity in vivo by inducing cell cycle arrest in G0/G1 phase and promoting cell apoptosis. Furthermore, we identified RegIV as a target of miR-24 and demonstrated that miR-24 regulated RegIV expression via binding its 3' untranslated region.&lt;h4>Conclusions&lt;/h4>miR-24 functions as a novel tumor suppressor in GC and the anti-oncogenic activity may involve its inhibition of the target gene RegIV. These findings suggest the possibility for miR-24 as a therapeutic target in GC.</pubmed_abstract><journal>Molecular cancer</journal><pagination>127</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4041902</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Tumor suppressor miR-24 restrains gastric cancer progression by downregulating RegIV.</pubmed_title><pmcid>PMC4041902</pmcid><pubmed_authors>Yan M</pubmed_authors><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Yu B</pubmed_authors><pubmed_authors>Li C</pubmed_authors><pubmed_authors>Zhu Z</pubmed_authors><pubmed_authors>Su L</pubmed_authors><pubmed_authors>Liu B</pubmed_authors><pubmed_authors>Hu L</pubmed_authors><pubmed_authors>Yang Q</pubmed_authors><pubmed_authors>Xiang M</pubmed_authors><pubmed_authors>Duan Y</pubmed_authors><pubmed_authors>Yu Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Tumor suppressor miR-24 restrains gastric cancer progression by downregulating RegIV.</name><description>&lt;h4>Background&lt;/h4>microRNAs are small noncoding RNAs that modulate a variety of cellular processes by regulating multiple targets, which can promote or inhibit the development of malignant behaviors. Accumulating evidence suggests miR-24 plays important roles in human carcinogenesis. However, its precise biological role remains largely elusive. This study examined the role of miR-24 in gastric cancer (GC).&lt;h4>Methods&lt;/h4>The expression of miR-24 in GC tissues compared with matched non-tumor tissues and GC cells was detected by qRT-PCR. Synthetic short single or double stranded RNA oligonucleotides and lentiviral vectors were used to regulate miR-24 expression in GC cells to investigate its function in vitro and in vivo.&lt;h4>Results&lt;/h4>miR-24 was significantly downregulated in GC tissues compared with matched non-tumor tissues and was associated with tumor differentiation. Ectopic expression of miR-24 in SGC-7901 GC cells suppressed cell proliferation, migration and invasion in vitro as well as tumorigenicity in vivo by inducing cell cycle arrest in G0/G1 phase and promoting cell apoptosis. Furthermore, we identified RegIV as a target of miR-24 and demonstrated that miR-24 regulated RegIV expression via binding its 3' untranslated region.&lt;h4>Conclusions&lt;/h4>miR-24 functions as a novel tumor suppressor in GC and the anti-oncogenic activity may involve its inhibition of the target gene RegIV. These findings suggest the possibility for miR-24 as a therapeutic target in GC.</description><dates><release>2014-01-01T00:00:00Z</release><publication>2014 May</publication><modification>2025-04-21T20:10:29.693Z</modification><creation>2019-03-27T01:29:19Z</creation></dates><accession>S-EPMC4041902</accession><cross_references><pubmed>24886316</pubmed><doi>10.1186/1476-4598-13-127</doi></cross_references></HashMap>