Knockdown of NCAPG promotes the apoptosis and inhibits the invasion and migration of triple‑negative breast cancer MDA‑MB‑231 cells via regulation of EGFR/JAK/STAT3 signaling
Affiliations: Department of Thyroid, Breast and Vascular Surgery, Shenzhen Longgang Central Hospital, Shenzhen, Guangdong 518116, P.R. China
- Published online on: February 1, 2023 https://doi.org/10.3892/etm.2023.11818
- Article Number: 119
Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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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.