Abstract
Effect of microRNA-27b (miR-27b) on cisplatin chemotherapy sensitivity of oral squamous cell carcinoma (OSCC) was investigated to provide a reference for clinical prevention of OSCC cell resistance. The clinical tissues of 34 patients with OSCC-resistant cancer and 28 patients with cisplatin-sensitive OSCC in Nanjing General Hospital were collected. The expression levels of miR-27b and Frizzled-7 (FZD7) in cancer tissues were detected by reverse transcription-quantitative polymerase chain reation (RT-qPCR). After a certain gradient of cisplatin was used to induce stable acquired resistance of OSCC cell line Tca8113/CDDP, a dose of miR-27b was added to construct a cell line overexpressing miR-27b in the drug-resistant cell line. The effect of cisplatin on the proliferation of drug-resistant OSCC cells was detected by colony formation assay. In addition, the scratch test and Transwell formation assay was performed to examine the effect of cisplatin drug stimulation on proliferation and migration of Tca8113/CDDP. Flow cytometry and Hoechst 33258 staining were used to detect the effect of miR-27b on apoptosis of OSCC-resistant cells after cisplatin chemotherapy. The expression level of miR-27b in cancer tissues of patients with drug-resistant OSCC was significantly lower than that of patients with OSCC cisplatin sensitivity (P<0.05). After high expression of miR-27b, the number of clones of drug-resistant OSCC cells after adding cisplatin drugs can be significantly inhibited. The proliferation and migration ability of drug-resistant OSCC was significantly decreased after the addition of cisplatin in miR-27b overexpression (P<0.05). miR-27 mimic enhanced the pro-apoptotic ability of cisplatin drugs (P<0.05). The expression of FZD7 in cisplation-resistant patients was significantly higher (P<0.05). miR-27b significantly inhibited the expression of FZD7 and β-catenin proteins. miR-27b can inhibit the resistance of OSCC to cisplatin drugs, increase apoptosis of cancer cells, and inhibit the proliferation of cancer cells. The mechanism may be related to the inhibition of FZD7/β-catenin signaling pathway activation in drug-resistant cell lines by miR-27b.