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Cleavage factor “CFIm25”, as a key repressor at proximal poly (A) site, negatively correlates to cell proliferation and tumorigenicity in various cancers. Hence, understanding CFIm25 mechanism of action in breast cancer would be a great benefit. To this aim four steps were designed. First, potential  miRNAs  that target 3′-UTR of  CFIm25  mRNA, retrieved from Targetscan web server. Second, screened  miRNAs  were profiled in 100 breast cancer and 100 normal adjacent samples. Third,  miRNAs  that their expression was inversely correlated to the CFIm25, overexpressed in MDA-MB-231 cell line, and their effect on proliferation and migration monitored via MTT and wound healing assays, respectively. Fourth, interaction of  miRNAs  of interest with 3′-UTR of  CFIm25  confirmed via luciferase assay and western blot. Our results indicate that  CFIm25  considerably down-regulates in human breast cancer tissue. qRT-PCR assay, luciferase test, and western blotting confirm that  CFIm25  itself could be directly regulated by oncomiRs such as  miR-23 ,  -24, -27, -135, -182  and  -374 . Besides, according to MTT and wound healing assays of cell lines,  CFIm25  knockdown intensifies cell growth, proliferation and migration. Our results also confirm indirect impact of CFIm25 on regulation of mRNA’s 3′–UTR length, which then control corresponding  miRNAs’  action.  miRNAs  directly control CFIm25 expression level, which then tunes expression of the oncogenes and tumor proliferation. Therefore, regulation of CFIm25 expression level via  miRNAs  is expected to improve treatment responses in breast cancer.

Involved microRNAs in alternative polyadenylation intervene in breast cancer via regulation of cleavage factor “CFIm25”