Silencing The Copb2 Gene Decreases The Proliferation, Migration And Invasion Of Human Triple-Negative Breast Cancer Cells

Triple-negative breast cancer (TNBC) is highly invasive, has a high rate of recurrence and is associated with a poor clinical outcome when compared with non-TNBC due to a lack of effective and targeted treatments. The coatomer protein complex subunit beta 2 (COPB2) is upregulated in various types of malignant cancer. The present study demonstrated that COPB2 expression levels were significantly upregulated in breast carcinoma HS-578T cells (clonal cells originating from TNBC) when compared with non-TNBC MCF-7 cells. HS-578T cells also exhibited higher rates of proliferation, invasion and transendothelial migration when compared with MCF-7 cells. Moreover, it was identified that genetically silencing the COPB2 gene using a lentivirus-short hairpin RNA inhibited the proliferative, colony formation, migratory and invasive properties of the TNBC HS-578T cells. Mediation of the COPB2 silencing effect may be associated with regulating the phosphorylation of serine/threonine kinase AKT in the PI3K/AKT signaling pathway. These results suggested the importance of COPB2 in promoting the proliferation of TNBC cells and identified COPB2 as a potential novel therapeutic target.