Abstract
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.
Highlights
Endometrial cancer, known as uterine corpus cancer, is one of the three major malignant tumors in gynecology, accounting for about 30% of malignant tumors of female reproductive tract [1]
BMI1 antibody was purchased from China Beyotime Biotech Co., Ltd. (Shanghai, China), small molecule BMI1 inhibitor (PTC-209) was purchased from Nanjing KeyGen Biotech Co., Ltd. (Nanjing, China); Roswell Park Memorial Institute 1640 (RPMI 1640) culture medium was purchased from Wuhan Promoter Biological Co., Ltd. (Wuhan, China); cell counting kit-8 (CCK-8) kit was purchased from China Beyotime Biotech Co., Ltd. (Shanghai, China); P53, P21, and Bax primary antibodies were all purchased from German Miltenyi Biotec Company (San Jose, CA, USA); fetal bovine serum was purchased from Hangzhou Sijiqing Company (Hangzhou, China); ELX800 microplate reader was purchased from American Bio-Tek Company (BioTek Winooski, VT, USA); and CO2 incubator was purchased from Nison Instrument (Shanghai) Limited (Shanghai, China)
Overexpression of BMI1 in Endometrial Cancer. Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) showed that the expression of BMI1 in endometrial cancer tissues was significantly higher than that in paracancerous tissues (P < 0.05), and IHC staining showed that the positive expression of BMI1 in endometrial cancer tissues was enhanced (P < 0.05) (Figure 1)
Summary
Endometrial cancer, known as uterine corpus cancer, is one of the three major malignant tumors in gynecology, accounting for about 30% of malignant tumors of female reproductive tract [1]. 90% of endometrial cancers are sporadic, and the remaining 10% are hereditary, which seriously affects women’s health and life [2]. Endometrial cancer most often occurs during perimenopause and postmenopause, and it undergoes complex dynamic changes under the action of hormones. The exact etiology of endometrial cancer still remains unknown. Clinical observation and research suggest that it may be related to the long-term continuous stimulation of estrogen on endometrium, endometrial hyperplasia, infertility, delayed menopause and late menopause, and family history [3]. Endometrial cancer often occurs in people with obesity, irregular menstruation, family history of tumor, and excessive estrogen supplementation. Hypertension, and diabetes may induce endometrial cancer [4]
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