<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>22(1)</volume><submitter>Phatak P</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>MicroRNA (miR)-214-3p is emerging as an important tumor suppressor in esophageal cancer. In this study, we examined the interaction between miR-214-3p and RAB14, a membrane trafficking protein shown to exert oncogenic functions in other malignancies, in esophageal cancer cells.&lt;h4>Methods&lt;/h4>Studies were performed in a human esophageal epithelial cell line and a panel of esophageal cancer cell lines, as well in human specimens. MiR-214-3p expression was measured by digital PCR. Biotinylated RNA pull-down and luciferase reporter assays assessed binding. The xCELLigence RTCA system measured cell migration and invasion in real time. A lentiviral expression vector was used to create an esophageal cancer cell line stably expressing miR-214-3p.&lt;h4>Results&lt;/h4>MiR-214-3p expression was decreased in esophageal cancer cell lines and human specimens compared to non-malignant controls. RAB14 mRNA stability and protein expression were decreased following miR-214-3p overexpression. Binding between miR-214-3p and RAB14 mRNA was observed. Either forced expression of miR-214-3p or RAB14 silencing led to a marked decrease in cellular migration and invasion. Esophageal cancer cells stably expressing miR-214-3p demonstrated decreased growth in a subcutaneous murine model.&lt;h4>Conclusions&lt;/h4>These results further support the tumor-suppressive role of miR-214-3p in esophageal cancer cells by demonstrating its ability to regulate RAB14 expression.</pubmed_abstract><journal>BMC cancer</journal><pagination>1265</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9721009</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>MiR-214-3p targets Ras-related protein 14 (RAB14) to inhibit cellular migration and invasion in esophageal Cancer cells.</pubmed_title><pmcid>PMC9721009</pmcid><pubmed_authors>Burrows WM</pubmed_authors><pubmed_authors>Phatak P</pubmed_authors><pubmed_authors>Youssef M</pubmed_authors><pubmed_authors>Donahue JM</pubmed_authors><pubmed_authors>Lee G</pubmed_authors><pubmed_authors>Creed TM</pubmed_authors></additional><is_claimable>false</is_claimable><name>MiR-214-3p targets Ras-related protein 14 (RAB14) to inhibit cellular migration and invasion in esophageal Cancer cells.</name><description>&lt;h4>Background&lt;/h4>MicroRNA (miR)-214-3p is emerging as an important tumor suppressor in esophageal cancer. In this study, we examined the interaction between miR-214-3p and RAB14, a membrane trafficking protein shown to exert oncogenic functions in other malignancies, in esophageal cancer cells.&lt;h4>Methods&lt;/h4>Studies were performed in a human esophageal epithelial cell line and a panel of esophageal cancer cell lines, as well in human specimens. MiR-214-3p expression was measured by digital PCR. Biotinylated RNA pull-down and luciferase reporter assays assessed binding. The xCELLigence RTCA system measured cell migration and invasion in real time. A lentiviral expression vector was used to create an esophageal cancer cell line stably expressing miR-214-3p.&lt;h4>Results&lt;/h4>MiR-214-3p expression was decreased in esophageal cancer cell lines and human specimens compared to non-malignant controls. RAB14 mRNA stability and protein expression were decreased following miR-214-3p overexpression. Binding between miR-214-3p and RAB14 mRNA was observed. Either forced expression of miR-214-3p or RAB14 silencing led to a marked decrease in cellular migration and invasion. Esophageal cancer cells stably expressing miR-214-3p demonstrated decreased growth in a subcutaneous murine model.&lt;h4>Conclusions&lt;/h4>These results further support the tumor-suppressive role of miR-214-3p in esophageal cancer cells by demonstrating its ability to regulate RAB14 expression.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Dec</publication><modification>2024-11-15T05:48:39.471Z</modification><creation>2024-11-15T05:48:39.471Z</creation></dates><accession>S-EPMC9721009</accession><cross_references><pubmed>36471277</pubmed><doi>10.1186/s12885-022-10304-0</doi></cross_references></HashMap>