CBX3 promotes ovarian cancer progression by regulating p53/p21-mediated glucose metabolism via inhibiting NCOR2

• Published in: Archives of medical science
• Main Authors: Chen, Hua, Han, Cailing, Liu, Dan, Wang, Fang, Ha, Chunfang
• Format: Journal Article
• Language: English
• Published: 03.08.2022
• ISSN: 1734-1922; 1896-9151
• DOI: 10.5114/aoms/149379

Introduction Chromobox protein homolog 3 (CBX3) has been reported to regulate a variety of cellular biological functions and play an oncogenic role in various tumor. Nevertheless, the role of CBX3 remains vague in ovarian cancer. This research aimed to assess the role and potential regulatory mechanism of CBX3 in ovarian cancer. Material and methods The CBX3 expression was determined by qRT-PCR and western blotting in ovarian cancer tissues and cell lines. Cell proliferation, cycle and apoptosis were detected by using CCK-8 assay and flow cytometry. Transwell and wound healing assay were used to determine cell invasion and migration. Furthermore, the modulation of CBX3 on NCOR2 expression and p53/p21-mediated glycolysis was confirmed. Results The expression of CBX3 was significant elevated in ovarian cancer tissues and cell lines. CBX3 knockdown inhibited cell proliferation, invasion and migration, while promoted G1/S phase blockade and cell apoptosis. Mechanism analysis verified that CBX3 downregulation increased NCOR2 expression and blocked subsequent p53/p21-mediated glucose metabolism. NCOR2 silencing and p53/p21 inhibitor treatment reversed the inhibitory effects of CBX3 knockdown on ovarian cancer cellular function. Conclusions We revealed that CBX3 promoted ovarian cancer progression by promoting p53/p21-mediated glucose metabolism via inhibiting NCOR2. These results provide a theoretical basis for the diagnosis and treatment of ovarian cancer.