The Effect of miR-372 on Genome Instability in MKN-45 Cell Line

Gastric cancer is one of the most common cancers in the world and the second leading cause of cancer mortality in humans. MicroRNAs are a group of endogenous RNA, small non-coding nucleotides in length 21-23. Overexpression of miR-372 acts as an oncomir in various types of cancer by down-regulation its target LATS2.Down-regulation of LATS2 leads to the loss of cell cycle regulation, apoptosis inhibition, and increased proliferation rate of cells. In this study, we increased the expression of miR-372 with lentivirus transduction inside the GC cell line MKN-45. After selection of positive cells, miR-372 and LATS2 expression levels were measured through Real Time PCR. Cytochalasin B blocked (MN) assay was done to verify the presence or absence of MN for comparing genomic instability in treated cells compared to the control cells. In the treated cells compared with control cells, the amount of miR-372 expression significantly increased. Fold changes in 7, 14 and 21 days after transduction were 7.85, 50.22 and 114.68 (P = 0.03). In contrast to the control cells the fold changes of LATS2 expression in these days were 0.39, 0.29 and 0.15 (P = 0. 016). In addition, compared with control cells the genomic instability of treated cells increased significantly (P < 0.001). These results indicate that in MKN-45 cell line, LATS2 is a target of miR. LATS2 is down-regulated with increased expression of miR-372. Reduce LATS2, leading to genomic instability during cell division and creates micronuclei and hence may be an important tumor suppressor.