Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer and the treatment options are extremely limited. Non-SMC condensing I complex subunit G (NCAPG) expression is upregulated in TNBC, but its specific regulatory mechanism in TNBC has not been previously reported. The expression levels of NCAPG in TNBC were analyzed using data obtained from the UALCAN database. RT-qPCR and western blotting were used to detect the expression of NCAPG in various breast cancer cell lines. The expression of NCAPG was knocked down, and cell viability was then detected using a CCK-8 assay, apoptosis was detected using a TUNEL assay, and the expression of the apoptosis-related proteins Bcl-2, Bax and Bad were detected by western blotting. Wound healing and Transwell assays were used to assess migration and invasion. Western blotting was also used to determine the expression levels of migration and invasion-related proteins MMP2 and MMP9, as well as EGFR/JAK/STAT3 pathway-related proteins. Following exogenous treatment with EGF and the JAK/STAT3 signaling pathway agonist colivelin, cell viability, apoptosis, invasion and migration were assessed. The expression of NCAPG in TNBC MDA-MB-231 cells was significantly increased. Inhibition of NCAPG inhibited the activity, promoted apoptosis, and inhibited the invasion and migration of TNBC MDA-MB-231 cells, potentially via regulation of the EGFR/JAK/STAT3 signaling pathway. In conclusion, downregulation of NCAPG can promote apoptosis and inhibit invasion and migration of TNBC MDA-MB-231 cells via EGFR/JAK/STAT3 signaling.

BackgroundAlthought lncRNA SEMA3B-AS1 was known to be involved in the development of many types of cancer, the role of SEMA3B-AS1 in triple-negative breast cancer (TNBC) remains unknown. This study was to investigate the role and underlying mechanism of SEMA3B-AS1 in TNBC.The mRNA expression of SEMA3B-AS1, miR-545 and CDK4 in TNBC tissues and non-cancer tissues of TNBC patients (n = 69) was detected by RT-qPCR. The protein expression of CDK4 was detected by Western blot. Cell proliferation were evaluated by CCK-8 assay.ResultsWe found that the expression of SEMA3B-AS1 was downregulated in TNBC tissues. The expression of SEMA3B-AS1 was positively correlated with the expression of miR-545 and inversely correlated with the expression of CDK4. Overexpression of SEMA3B-AS1 or miR-545 resulted in the downregulation of CDK4. Moreover, miR-545 inhibitor attenuated the effect of SEMA3B-AS1 overexpression on CDK4 expression. SEMA3B-AS1 overexpression also resulted in the upregulation of miR-545. Overexpression of SEMA3B-AS1 or miR-545 decreased the rate of TNBC cell proliferation, while overexpression of CDK4 increased the rate of TNBC cell proliferation. In addition, miR-545 inhibitor attenuated the effect of SEMA3B-AS1 overexpression on cell proliferation.Interaction between SEMA3B-AS1 and CDK4 mediated by miR-545 regulates the proliferation of TNBC cells.