Evading apoptosis—a hallmark of cancer—is highly dependent on BCL-21-4
Haematological malignant cells are able to survive and thrive when there is an imbalance of BCL-2 family proteins3
Unlike normal cells, cancer cells divide and grow uncontrollably—not only by impairing normal cellular growth but also by evading apoptosis.1
- The dynamic balance between free pro-apoptotic proteins and anti-apoptotic proteins, such as BCL-2, BCL-XL, and MCL-1, determines whether the cancer cell undergoes or evades apoptosis1,4
- BCL-2–dependent apoptosis evasion can enable tumour development and the potential for cancer therapy resistance1,4
The principal function of the BCL-2 protein is to bind and sequester pro-apoptotic proteins, limiting their ability to initiate apoptosis.2
BCL-2=B-cell lymphoma 2; BCL-XL=B-cell lymphoma-extra large; MCL-1=myeloid cell leukaemia 1.
References: 1. Adams JM, Cory S. The Bcl-2 apoptotic switch in cancer development and therapy. Oncogene. 2007;26(9):1324-1337. 2. Plati J, Bucur O, Khosravi-Far R. Apoptotic cell signaling in cancer progression and therapy. Integr Biol (Camb). 2011;3(4):279-296. 3. Reed JC. Bcl-2–family proteins and hematologic malignancies: history and future prospects. Blood. 2008;111(7):3322-3330. 4. Fernald K, Kurokawa M. Evading apoptosis in cancer. Trends Cell Biol. 2013;23(12):620-633.