Bax is involved in the anticancer activity of Velcade in colorectal cancer

Numerous chemotherapeutic agents promote tumor cell death by activating the intrinsic apoptosis signaling pathway. This pathway is regulated by mitochondrial dysfunction, which occurs through an intricate process controlled by complex interactions between B-cell lymphoma 2 (Bcl-2) family members and other cellular proteins. Bcl-2-associated X protein (Bax) is a proapoptotic protein that is an essential component of the intrinsic apoptosis signaling pathway. Patients lacking Bax may be less sensitive to chemotherapy due to an impaired intrinsic apoptosis signaling pathway. The present study demonstrated that Bax expression in colorectal cancer (CRC) tissues was typically increased compared with that in adjacent normal tissues. Furthermore, Bax^-/- HCT-116 cells exhibited reduced proliferation and colony formation ability compared with Bax^+/+ HCT116 cells, although the rate of apoptosis of these cells remained unchanged. However, Bax^-/- HCT116 cells became more resistant to apoptosis when treated with Velcade. The results of the present study provide novel insights into the relevance of Bax expression to the prognosis of CRC.