MicroRNA-143 Sensitizes Cervical Cancer Cells to Cisplatin: a Promising Anticancer Combination Therapy

Cellular landscaping of cisplatin resistance in cervical cancer

“…This research shows that TBX1, a miR-6727-5p target gene, works as a tumour suppressor in CC, suggesting that TBX1 could be a potential target for therapy of CC [234]. Esfandyari et al showed that the overexpression of miRNA-143 induces apoptosis by CDDP and enhance the susceptibility to lower dosage of CDDP by regulating the expression of genes related to apoptosis such as caspase-9, Bax, and Bcl-2 by overexpression of miRNA-143 [235]. After CDDP treatment, Shi et al found that overexpression of miR-144 by binding with the 3 ′ -UTR of LHX2 lowered cell viability, triggered cell death, and hindered cell migration and invasion in CC.…”

Cisplatin for cancer therapy and overcoming chemoresistance

“…Cisplatin treatment delivered in combination with photodynamic therapy (using lasers with methylene blue as the photosensitizing agent) to cervical cancer cell lines, A2780 (sensitive to cisplatin) and A2750-CP (resistant to cisplatin) enhanced drug sensitivity by decreasing the half-maximal inhibitory level (IC 50 ) by 2-fold that caused cell membrane disruption through lipid peroxidation [ 204 ]. miR143 was found to synergise cisplatin activity in CaSki cell line which are derived from cervical cancers by the upregulation of the apoptosis-related genes Bax, BCl-2 and caspase 9 [ 205 ]. miR143 was overexpressed in chemo-sensitive cells which together with cisplatin increased cell cycle arrest at the sub-G1 and G2-M phases, induced autophagy activation, downregulated vimentin - inhibited CaSki cell migration and c-Myc expression in the treatment group [ 205 ].…”

“…miR143 was found to synergise cisplatin activity in CaSki cell line which are derived from cervical cancers by the upregulation of the apoptosis-related genes Bax, BCl-2 and caspase 9 [ 205 ]. miR143 was overexpressed in chemo-sensitive cells which together with cisplatin increased cell cycle arrest at the sub-G1 and G2-M phases, induced autophagy activation, downregulated vimentin - inhibited CaSki cell migration and c-Myc expression in the treatment group [ 205 ]. A tumour -suppressor transcription factor ZBTB28 (which is often silenced in cervical cancer cells by CpG methylation of its promoter) was identified as a potential therapeutic target in cervical cancer that increased chemosensitivity to cisplatin therapy [ 206 ].…”

MicroRNAs as the critical regulators of autophagy-mediated cisplatin response in tumor cells

“…Interestingly, the combined miR-143 and cisplatin treatment resulted in autophagy induction, cell cycle arrest, c-Myc downregulation, and cell migration suppression by vimentin down regulation. Therefore, application of miR-143 in conjunction with cisplatin may provide a potential therapeutic approach for cervical cancer patients [ 106 ]. MiR-7-5p was found to be upregulated in cisplatin-resistant cervical tumor cells, boosting energy production via targeting Bcl-2 and decreasing energy consumption through PARP-1 targeting.…”