A potential role of nuclear matrix-associated protein kinase CK2 in protection against drug-induced apoptosis in cancer cells

Protein kinase CK2 (CK2) has long been implicated in the regulation of cell growth and proliferation. Its activity is generally elevated in rapidly pr oliferating tissues, and nuclear matrix (NM) is an important subnuclear loc ale of its functional signaling. In the prostate, nuclear CK2 is rapidly lo st commensurate with induction of receptor-mediated apoptosis after growth stimulus withdrawal. Ey contrast, chemical-induced apoptosis in prostate ca ncer and other cells (by etoposide and diethylstilbestrol) evokes an enhanc ement in CK2 associated with the NM that appears to be because of transloca tion of CK2 from the cytoplasmic to the nuclear compartment. This shuttling of CK2 to the NM may reflect a protective response to chemical-mediated ap optosis. Supporting evidence for this was obtained by employing cells that were transiently transfected with various expression plasmids of CK2 (there by expressing additional CK2) prior to treatment with etoposide or diethyls tilbestrol. Cells transfected with the CK2 alpha or CK2 alpha beta showed s ignificant resistance to chemical-mediated apoptosis commensurate with the corresponding elevation in CK2 in the NM. Transfection with CK2 beta did no t demonstrate this effect. These results suggest, for the first time, that besides the commonly appreciated function of CK2 in cell growth, it may als o have a role in protecting cells against apoptosis.