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ABSTRACT
To study the effect of miR-200a on radiosensitivity of osteosarcoma cells and its mechanism. NC (normal cell) group, mimic-NC group, mimic-miR-200a group, inhibitor-NC group, inhibitor-miR-200a group, si-NC group, si-BMPR2 (Bone morphogenetic protein receptor 2) group, mimic-miR-200a+vector-NC group, and mimic-miR-200a+vector-BMPR2 group were set; the cells of the above groups were irradiated with different radiation intensities (0, 1, 2, 3, and 4 Gy). The expression of miR-200a and BMPR2 mRNA was detected by qRT-PCR; the expression of BMPR2 protein was detected by Western blot; cell viability was detected by MMT (3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide); apoptosis rate was detected by flow cytometry. Cell clone formation experiment was used to detect cell radiosensitivity. Dual-luciferase reporter gene test was used to detect cell fluorescence activity. The expression of BMPR2 was high and the expression of miR-200a was low in osteosarcoma tissues after radiotherapy and in osteosarcoma cells after irradiation. Overexpression of miR-200a and interference with BMPR2 expression inhibits osteosarcoma cell proliferation, promotes apoptosis, and increases cellular radiosensitivity, miR-200a targets expression of BMPR2, and overexpression of BMPR2 reverses the radiosensitizing and apoptotic effects of miR-200a expression on osteosarcoma cells. Overexpression of miR-200a inhibits osteosarcoma cell proliferation, promotes apoptosis, and increases cellular radiosensitivity. The mechanism may be related to the regulation of BMPR2, which may provide new targets and new ideas for osteosarcoma treatment.
Disclosure statement
No potential conflict of interest was reported by the author(s).