Abstract
Exploring new diagnostic biomarkers and molecular targets is of great importance in breast cancer treatment. The present study investigated the effects of acetyl-CoA carboxylase (ACC) expression interference on the malignant progression of breast cancer cells. ACC expression was knocked down using a lentiviral vector and this was verified by quantitative polymerase chain reaction and western blotting. MCF-7 and MDA-MB-231 breast cancer cells were randomly allocated into the following groups: Normal breast cancer cells (control), breast cancer cells transduced with a negative control lentiviral vector and breast cancer cells transduced with an ACC knockdown lentiviral vector. Screening for stable transgenic strains was successful. Cell viability, apoptosis and migration were determined using Cell Counting Kit-8, flow cytometry and scratch test, respectively. The protein expression levels of N-cadherin, Vimentin and Bax were detected by western blotting. In addition, a nude mouse model of subcutaneous metastatic tumor was established using MCF-7 breast cancer cells, and tumor volume was assessed. Furthermore, pathological condition and apoptosis were detected using hematoxylin and eosin, and TUNEL staining, respectively. The protein expression levels of N-cadherin, Vimentin and Bax were detected by western blotting. The in vitro experiments showed that knockdown of ACC expression significantly decreased the viability and migration, and increased the apoptosis of MCF-7 and MDA-MB-231 breast cancer cells. In vivo experiments revealed that ACC knockdown effectively reduced the tumor volume in nude mice, and promoted tumor cell apoptosis. Both in vitro and in vivo experiments showed that ACC knockdown can reduce the protein expression levels of N-cadherin and Vimentin, and increase Bax expression. These findings suggested that downregulation of ACC expression may significantly reduce the malignant progression of breast cancer, and could be considered a potential therapeutic target.