Nayer Hosseinahli
1 
, Tahereh Zeinali
1,2, Nasrin Hosseinahli
3, Leila Karimi
1, Dariush Shanehbandi
1,4, Behzad Mansoori
1,4, Ali Mohammadi
1, Tohid Kazemi
5, Khalil Hajiasgharzadeh
1,6, Behzad Baradaran
1,5* 1 Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
2 Gastrointestinal and Liver Diseases Research Center, Guilan University of Medical Sciences, Rasht, Iran.
3 Azarbaijan Higher Education and Research Complex, Tabriz, Iran.
4 Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran.
5 Department of Immunology, Tabriz University of Medical Sciences, Tabriz, Iran.
6 Connective Tissue Diseases Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Abstract
Purpose: Gastric cancer (GC) is one of the main causes of death from diseases, especially indeveloping countries. MicroRNAs (miRNAs) are important modulators of the messenger RNAsexpression. Among these miRNAs, MiR-143 is a tumor suppressor miRNA and its irregularexpression has been revealed in a diversity of malignancies such as GC.Methods: In this study, we have attempted to restore the miR-143 expression in MKN-45 cellsby introducing pCMV-miR-143 plasmid vectors. The consequences of exogenous expression ofmiR-143 on cell proliferation and migration were assessed by MTT and scratch tests, respectively.In addition, the DAPI staining assay was applied for apoptosis quantification. Following miR-143 transfection, the changes in K-Ras, C-Myc, MMP9, Bax, caspase-3, and caspase-9 mRNAlevels were assessed.Results: The results indicated that the enhanced expression of miR-143 had negative effects onMKN-45 cells proliferation and invasion. Moreover, decreased expressions of K-Ras, MMP9,and C-Myc and up-regulation of Bax, caspase-3, and caspase-9 as downstream targets of miR-143 were recognized.Conclusion: These experimental results indicate that reversing the miR-143 expression, by noveltechniques, including miRNA replacement could be considered as an efficient approach toreduce cell survival and metastasis.