The effect of miR-1226-3p on breast cancer

Breast cancer is the leading cause of cancer-related mortality among women worldwide. In Iran, breast cancer ranks first among cancers diagnosed in women comprising 24.4% of all malignancies. Currently, the large number of etiological factors and the complexity of breast cancer present challenge for prevention and treatment. Breast cancer tumorigenesis can be described as a multi-step process in which a normal cell undergoes malignant transformation to a fully developed tumor through accumulations of genetic and epigenetic changes. On the other hand, several studies indicated the signaling pathways role in Breast cancer. EGFR gene has been shown to be overexpressed in breast cancer. Dimerization of EGFR/HER2 induces breast cancer progression via activation of PI3K/AKT signaling cascade. MicroRNAs are endogenous, small non-coding RNAs that regulate gene expression at the transcriptional and posttranscriptional level. MicroRNAs pair with partially complementary sites in the 3′untranslated regions (UTRs) of target mRNAs, leading to translational repression and/or mRNA degradation. In present study we applied bioinformatics data to predict miR-1226-3p as the regulator of PI3K/AKT pathway. Then significant down regulation of three target genes EGFR, PIK3R5 and AKT2 was observed post transfection of miR-1226-3p. To validate the effect of this down regulation on cells, expression of downstream genes PCNA, C-MYC and CCND1 was evaluated. Down regulation of these genes demonstrated that cell proliferation in this breast cancer cell line was inhibited and this miRNA could be considered as a tumor suppressor.