MicroRNA-216a-5p inhibits the development of gastric cancer through target combination with TCTN1.

Abstract

We aimed at investigating microRNA-216a-5p expression in gastric cancer (GC) tissues and further exploring whether microRNA-216a-5p suppresses GC progression through interacting with TCTN1. microRNA-216a-5p expression in 60 pairs of GC tissues and adjacent ones was studied by quantitative real-time polymerase chain reaction (qRT-PCR) analysis, and the relationship between microRNA-216a-5p and clinical indicators as wells as prognosis of GC patients was also analyzed. At the same time, qRT-PCR was conducted to further verify microRNA-216a-5p level in GC cells. The impacts of microRNA-216a-5p on GC cell functions were evaluated using cell counting kit-8, plate cloning and Transwell experiments. Meanwhile, we studied the specific regulatory relationship between microRNA-216a-5p and TCTN1 in depth. Our data showed that microRNA-216a-5p level in GC tumor specimens was remarkably lower than that in adjacent ones. In comparison to patients in group of high microRNA-216a-5p expression, patients in group of low expression showed an increased metastasis incidence and a lower survival rate. Cell functional experiments suggested that microRNA-216a-5p mimics markedly attenuated the proliferative and migratory capacities of GC cells. Bioinformatics analysis suggest that microRNA-216a-5p can bind to its target gene TCTN1, which was confirmed by luciferase assay. Further, qPCR results revealed a negative correlation between the expression of TCTN1 and microRNA-216a-5p in GC tumor tissues. Finally, in vitro cell experiments suggested that overexpression of TCTN1 could reverse the inhibitory impact of upregulation of microRNA-216a-5p on GC cell functions. microRNA-216a-5p, abnormally lowly expressed in GC tissues, is markedly relevant to the high metastasis incidence and the poor prognosis of GC patients; in addition, microRNA-216a-5p inhibited GC's migration and proliferation capabilities through regulating TCTN1.