Pu, YouguangZhao, FangfangWang, HaiyanCai, WenjingCai, ShanbaoFi, Qiyi2017-06-072017-06-072016-08-05Pu, Y., Yi, Q., Zhao, F., Wang, H., Cai, W., & Cai, S. (2016). MiR-20a-5p represses multi-drug resistance in osteosarcoma by targeting the KIF26B gene. Cancer Cell International, 16, 64. http://doi.org/10.1186/s12935-016-0340-3https://hdl.handle.net/1805/12878BACKGROUND: Chemoresistance hinders curative cancer chemotherapy in osteosarcoma (OS), resulting in only an approximately 20 % survival rate in patients with metastatic disease at diagnosis. Identifying the mechanisms responsible for regulating chemotherapy resistance is crucial for improving OS treatment. METHODS: This study was performed in two human OS cell lines (the multi-chemosensitive OS cell line G-292 and the multi-chemoresistant OS cell line SJSA-1). The levels of miR-20a-5p and KIF26B mRNA expression were determined by quantitative real-time PCR. KIF26B protein levels were determined by western blot analysis. Cell viability was assessed by MTT assay. Apoptosis was evaluated by flow cytometry. RESULTS: We found that miR-20a-5p was more highly expressed in G-292 cells than in SJSA-1 cells. Forced expression of miR-20a-5p counteracted OS cell chemoresistance in both cell culture and tumor xenografts in nude mice. One of miR-20a-5p's targets, kinesin family member 26B (KIF26B), was found to mediate the miR-20a-5p-induced reduction in OS chemoresistance by modulating the activities of the MAPK/ERK and cAMP/PKA signaling pathways. CONCLUSIONS: In addition to providing mechanistic insights, our study revealed that miR-20a-5p and KIF26B contribute to OS chemoresistance and determined the roles of these genes in this process, which may be critical for characterizing drug responsiveness and overcoming chemoresistance in OS patients.en-USAttribution-NonCommercial-NoDerivs 3.0 United StatesOsteosarcomamiR-20a-5pKIF26BMulti-drug resistanceArticle