Knockdown of CSNK2β suppresses MDA-MB231 cells growth, induces apoptosis, inhibits migration and invasion

Breast cancer is most common cancer among women worldwide and among different types of breast cancer treatment of triple-negative breast cancer is major challenge, thus identification of specific drivers is required for targeted therapies of this malignancy. The aim of the present study is to elucidate the effects of silencing of CSNK2{beta} gene by small interfering RNA (siRNA) on proliferation, cell cycle and apoptosis in breast carcinoma MDA MB-231 cells. Silencing of CSNK2{beta} in MDA-MB-231(a triple negative cell line) cells resulted in decreased cell viability and colony formation. Cell cycle analysis showed that silencing of CSNK2{beta} arrested MDA MB-231 cells in G2/M phase. We demonstrated that silencing of CSNK2{beta} promoted nuclear condensation and augmented intracellular ROS production. Furthermore, Silencing of CSNK2{beta} in MDA-MB 231 cells modulated the apoptotic machinery- BAX, Bcl-xL and caspase 3; autophagy machinary-Beclin-1 and LC3-1; and inhibited the vital markers (p-ERK, c-Myc, NF-{kappa}B, E2F1, PCNA, p38-) associated with cell proliferation and DNA replication pathways. In addition, Knocking down of CSNK2 {beta} also affected the migration potential of MDA-MB231 as observed in the wound healing and transwell migration assays. Together, our study suggests that CSNK2{beta} silencing may offer future therapeutic target in triple negative breast cancer.