The CTIP‐mediated repair of TNF‐α‐induced DNA double‐strand break was impaired by miR‐130b in cervical cancer cell

Chemotherapeutic drugs that induce DNA damage have the potential to kill cancer cells, but DNA repair protects cells from damage‐induced cell death. Thus, eliminating DNA repair is a potential approach to overcome cell drug resistance. In this study, we observed that the gene expression of C‐terminal binding protein interacting protein (CTIP) was promoted by TNF‐α stimulation and prevented TNF‐α‐induced double‐strand breaks (DSBs) in the genomes of cervical cancer cells. The putative miR‐130b targeted site within 3′ untranslated region (UTR) of CTIP mRNA was identified through in silico analysis and confirmed based on experimental data. By targeting the CTIP gene, miR‐130b caused the accumulation of DSBs and accelerated cell apoptosis in combination with poly ADP ribose polymerase (PARP) inhibitors. Additionally, overexpression of the CTIP gene elevated cancer cell viability by promoting proliferation while miR‐130b antagonized CTIP‐stimulated cell reproduction. Consequently, miR‐130b destruction of DNA repair should be employed as a strategy to treat cervical cancer.