Involvement of protein kinase C-delta in DNA damage-induced apoptosis

Abstract

Apoptosis is a highly orchestrated cell suicidal program required to maintain a balance between cell proliferation and cell death. A defect in apoptotic machinery can cause cancer. Many anticancer drugs are known to kill tumor cells by inducing apoptosis, and a defect in apoptosis can lead to anticancer drug resistance. Apoptosis is regulated by a complex cellular signaling network. Several members of the protein kinase C (PKC) family serve as substrates for caspases and PKCdelta isozyme has been intimately associated with DNA damage-induced apoptosis. It can act both upstream and downstream of caspases. In response to apoptotic stimuli, the full-length and the catalytic fragment of PKCdelta may translocate to distinct cellular compartments, including mitochondria and the nucleus, to reach their targets. Both activation and intracellular distribution of PKCdelta may have significant impact on apoptosis. This review intends to assimilate recent views regarding the involvement of PKCdelta in DNA damage-induced apoptosis.