miR-148-3p inhibits gastric cancer cell malignant phenotypes and chemotherapy resistance by targeting Bcl2.

Gastric cancer(GC) is the fourth most common cancer in the world. This work was designed to explore the biological effects of miR-148-3p on GC. Quantitative reverse transcription-polymerase chain reaction (RT-qPCR) was utilized to analyze the mRNA expression of miR-148-3p in GC cell lines. The mimics and inhibitors of miR-148-3p, was carefully transfected into GC cells to up-regulate or down-regulate miR-148-3p expression. Observe the effect on miR-148-3p expression change to GC cell proliferation, colony formation, tumorigenesis, chemotherapy sensitivity, trans-well migration and invasion. Use online database tool to predict the miR-148-3p promising targets, and be verified via RT-qPCR, Western blot and luciferase report. We found that miR-148-3p expression level in GC cells was markedly down-regulated (P <0.05), as compared with human normal gastric mucosal cells GES-1. Otherwise, miR-148-3p overexpression could effectively inhibit the cell proliferation, cell cycle progress, colony formation, anti-apoptosis, anti-migration and anti-invasion in gastric cancer cells, whereas miR-148-3p inhibition exhibited the opposite phenomenon (P<0.05). Further research revealed that Bcl2 set as a direct downstream target of miR-148-3p. Our study firstly confirmed that, miR-148-3p might play a crucial role in tumorigenesis, as well as development of gastric cancer by targeting Bcl2, and could become a promising target for gastric cancer treatment.

MiR-124-5p Inhibits the Progression of Gastric Cancer by Targeting MIEN1.

OBJECTIVE: To observe the effect of miR-124-5p on progression of gastric cancer (GC) and explore the targeting mechanism. METHODS: After collecting the specimens, we used real-time fluorescence quantitative PCR to detect the miR-124-5p level of GC tissue and corresponding adjacent tissue. Then MTT test and scratch wound-healing assay were hired to evaluate the influence of miR-124-5p in GC cell (SGC-803 and SGC7901) migration and proliferation ability. The binding of miR-124-5p to migration and invasion enhancer 1 (MIEN1) was detected through dual luciferase reporter gene experiment and western blot was utilized to assay the protein level of MIEN1. RESULTS: Compared with adjacent tissues, miR-124-5p level in GC tissues was lower significantly. MiR-124-5p mimic inhibited the metastasis and proliferation ability of SGC7901 cells and miR-124-5p inhibitor promoted the migration and proliferation ability of SGC803 cells. In addition, miR-124-5p targeted MIEN1 and negatively modulated the MIEN1 expression in SGC-803 and SGC7901 cells. Silencing MIEN1 negatively regulated the metastasis and proliferation ability of SGC7901 cells. CONCLUSION: MiR-124-5p inhibited the GC cell proliferation and metastasis phenotypes through MIEN1, which probably becomes a novel molecular target for clinical GC treatment.