Background: 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 of 21-23. Overexpression of miR-372 acts as an oncomir in various types of
cancer via down-regulation of its target, LATS2. Down-regulation of LATS2 leads to the loss of cell
cycle regulation, apoptosis inhibition, and increased proliferation rate of the cells.
Methods: 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 polymerase chain reaction (RT-PCR) assay. 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 controls.
Findings: In the treated cells, compared with the controls, the amount of miR-372 expression
significantly increased. Fold changes in 7, 14 and 21 days after the transduction were 7.85, 50.22 and
114.68, respectively (P = 0.030). In contrast to the control cells, the fold changes of LATS2 expression
in these days were 0.39, 0.29 and 0.15, respectively (P = 0. 016). In addition, compared with control
cells, the genomic instability of treated cells increased significantly (P < 0.001).
Conclusion: These results indicate that in MKN-45 cell line, LATS2 is a target of miR-372. LATS2 is
down-regulated with increased expression of miR-372. Reduce LATS2, leads to genomic instability
during cell division and creates micronuclei and hence may be an important tumor suppressor
