MiR-26a-5p Heightens Breast Cancer Cell Sensitivity to Paclitaxel via Targeting Flap Endonuclease 1

Objective Flap endonuclease 1 (FEN1) has been confirmed to involve the drug resistance of multiple cancers including breast cancer.However, the effect of miRNA-mediated FEN1 on breast cancer cell resistance is still ambiguous and needs further research. Methods Firstly, we used GEPIA2 to predict the FEN1 expression in breast cancer. Next, we used quantitative real-time polymerasechain reaction (qRT-PCR) and western blot to evaluate the FEN1 level of cells. After parental cells or MDA-MB-231-paclitaxel(PTX) cells being transfected with or without siFEN1, the apoptosis, migration, and protein levels of FEN1, Bcl-2, and resistance-relatedgenes were examined by flow cytometry, wound healing assay, and western blot, respectively. Then, the putative miRNA targetingFEN1 was predicted using StarBase V3.0, and further confirmed by qRT-PCR. The targeted binding of FEN1 to miR-26a-5p was detectedby dual-luciferase reporter assay. After parental cells or MDA-MB-231-PTX cells being transfected with or without miR-26a-5pmimic, the apoptosis, migration, and protein levels of FEN1, Bcl-2, and resistance-related genes were tested again. Results FEN1 expression was enhanced in breast cancer and MDA-MB-231-PTX cells. The combined application of FEN1 knockdown and PTXenhanced apoptosis in MDA-MB-231-PTX cells but suppressed cell migration and expressions of FEN1, Bcl-2, and resistance-relatedgenes. Then, we confirmed that FEN1 was targeted by miR-26a-5p. The combined application of miR-26a-5p mimic and PTX largelyfacilitated apoptosis in MDA-MB-231-PTX cells but restrained cell migration and expressions of FEN1, Bcl-2, and resistance-relatedgenes. Conclusion MiR-26a-5p contributes to the sensitivity of breast cancer cells to paclitaxel via restraining FEN1.