Silencing the COPB2 gene decreases the proliferation, migration and invasion of human triple‑negative breast cancer cells

Abstract

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 β2 (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.

Upregulation of COPB2 Promotes Prostate Cancer Proliferation and Invasion Through the MAPK/TGF-β Signaling Pathway

“…After so many researches, the differential and functional COPB2 protein was identified. COPB2 is involved in material transport, energy metabolism as a vesicular envelope protein and tumor progression (15,(26)(27)(28).…”