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The aim of this study was to examine the role of B lymphoma Moloney murine leukemia virus insertion region 1 (BMI1) gene in regulating the apoptosis, invasion, and migration of human endometrial adenocarcinoma cell line (HEC-1B) cells induced by ionizing radiation. The expression of BMI1 mRNA was detected by quantitative real-time polymerase chain reaction (qRT-PCR), and the positive expression of BMI1 was detected by immunohistochemistry (IHC) staining. HEC-1 B cells were randomly divided into three groups: control group, BMI1 overexpression group, and BMI1 inhibitor group. Cell proliferation was detected by cell counting kit-8 (CCK-8); cell migration and invasion were detected by Transwell test; cell apoptosis was detected by flow cytometry; and the expression of MMP2, MMP7, MMP9, Rock1, RhoA, P53, P21, and Bax protein was detected by the western blot. The results suggested that the expression of BMI1 mRNA and tissue positive in endometrial cancer tissues was increased significantly. After ionizing radiation, compared with the control group, the proliferation, cell migration, and invasion of HEC-1B cells were increased significantly in the BMI1 overexpression group, while the proliferation, cell migration, and invasion of HEC-1B cells were decreased significantly in BMI1 inhibitor group. The apoptosis rate of BMI1 overexpression group was decreased significantly, while the BMI1 inhibitor group was increased significantly. The levels of MMP2, MMP7, MMP9, Rock1, RhoA and p53, p21, Bax protein in BMI1 overexpression group were significantly increased, while the levels of MMP2, MMP7, MMP9, Rock1, RhoA and p53, p21, Bax protein in BMI1 inhibitor group were significantly decreased. BMI1 is highly expressed in endometrial cancer tissues, and inhibiting BMI1 expression can reduce the proliferation, migration, and invasion of HEC-1B cells after ionizing radiation and promote apoptosis, which offers new insights into the clinical radiotherapy of tumors.

Effects of BMI1 Gene on Regulating Apoptosis, Invasion, and Migration of HEC-1B Cells Induced by Ionizing Radiation