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Archive > Volume 26 Issue 10 > 2019,26(10):1107-1112. DOI:10.3872/j.issn.1007-385X.2019.10.009 Prev Next
Basic Research
miR-520a-3p enhances the paclitaxel sensitivity of non-small cell lung cancer A549/TAX cells by targeting FZD8
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Abstract:
[Abstract] Objective: To investigate the influence of miR-520a-3p on paclitaxel (TAX) sensitivity of non-small cell lung cancer (NSCLC) A549/TAX cells via regulating frizzled class receptor 8 (FZD8). Methods: NSCLC A549 cells, TAX-resistant cell line A549/TAX and human lung epithelial HLF-α cells were selected. The expression level of miR-520a-3p in A549 and A549/TAX cells was detected by qPCR. According to different transfection plasmids, the experimental cells were divided into control group, miR-520a-3p mimics group, si-FZ8 group and si-FZD8+miR-520a-3p inhibitor group. After being treated with 6 μmol/L paclitaxel, the proliferation of A549/TAX cells was determined by CCK-8 assay. Flow cytometry with Annexin V-FLTC/PI staining was used to detect the apoptosis level of A549/TAX cells. The expression of FZD8 in A549/TAX cells was detected by WB. The targeting relationship between miR-520a-3p and FZD8 was verified by the dual-luciferase reporter gene system. Results: miR-520a-3p was poorly expressed in TAX-resistant A549/TAX cells (P<0.01), and TAX up-regulated the expression of miR-520a-3p in A549/TAX cells (P<0.01). After the treatment with 6 μmol/L TAX, over-expression of miR-520a-3p significantly inhibited the proliferation of A549/TAX cells and promoted apoptosis (all P<0.01). Dual luciferase reporter gene assay showed that miR-520a-3p targetedly down-regulated the expression of FZD8 (P<0.01). si-FZD8 could significantly inhibit the proliferation and promote cell apoptosis of A549 / TAX cells, thereby enhancing the TAX sensitivity of cells. At the same time, simultaneous knockdown of miR-520a-3p and FZD8 could reverse the enhancement of FZD8 knockdown on TAX sensitivity of A549/TAX cells (P<0.01). Conclusion: miR-520a-3p enhances the TAX sensitivity of A549/TAX cells by down-regulating the expression of FZD8.
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