Published online Aug 21, 2015. doi: 10.3748/wjg.v21.i31.9337
Peer-review started: March 12, 2015
First decision: March 26, 2015
Revised: June 17, 2015
Accepted: July 8, 2015
Article in press: July 8, 2015
Published online: August 21, 2015
Processing time: 162 Days and 13.4 Hours
AIM: To elucidate the potential biological role of miR-30b in gastric cancer and investigate the underlying molecular mechanisms of miR-30b to inhibit metastasis of gastric cancer cells.
METHODS: The expression of miR-30b was detected in gastric cancer cell lines and samples by reverse transcription-polymerase chain reaction. CCK-8 assays were conducted to explore the impact of miR-30b overexpression on the proliferation of gastric cancer cells. Flow cytometry was used to examine the effect of miR-30b on the apoptosis. Transwell test was used for the migration and invasion assays. Luciferase reporter assays and Western blot were employed to validate regulation of putative target of miR-30b.
RESULTS: The results showed that miR-30b was downregulated in gastric cancer tissues and cancer cell lines and functioned as a tumor suppressor. Overexpression of miR-30b promoted cell apoptosis, and suppressed proliferation, migration and invasion of the gastric cancer cell lines AGS and MGC803. Bioinformatic analysis identified the 3’-untranslated region of eukaryotic translation initiation factor 5A2 (EIF5A2) as a putative binding site of miR-30b. Luciferase reporter assays and Western blot analysis confirmed the EIF5A2 gene as a target of miR-30b. Moreover, expression levels of the EIF5A2 targets E-cadherin and Vimentin were altered following transfection of miR-30b mimics.
CONCLUSION: Our findings describe a link between miR-30b and EIF5A2, which plays an important role in mediating epithelial-mesenchymal transition.
Core tip: In this study, we found that miR-30b expression was reduced in gastric cancer cell lines and in gastric cancer tissues. Moreover, we found that miR-30b inhibited gastric cancer cell proliferation, migration, invasion and promoted apoptosis by targeting EIF5A2. Restoration of miR-30b expression could enhance E-cadherin and β-catenin expression and suppress Vimentin expression by targeting EIF5A2 and eventually inhibit the epithelial-to-mesenchymal transition (EMT) process in gastric cancer cells, whereas knockdown of miR-30b promoted cell invasion and EMT in cancer cells.