Response of cancer cells to molecular interruption of the CK2 signal

Protein kinase CK2 is one of the key cellular signals for cell survival, gr owth, and proliferation. It is has been observed to be elevated in various cancers that have been examined. Various observations suggest that moderate dysregulation of CK2 may profoundly influence the cell response. We have e xamined the effects of interfering with the CK2 signal in various cancer ce ll lines by employing antisense oligodeoxynucleotides (ODN) against the alp ha and beta subunits of CK2. Our results demonstrate that antisense CK2-alp ha and antisense CK2-beta ODNs markedly influence cell viability of these c ancer cells in a dose and time-dependent manner. Antisense CK2-alpha was sl ightly more effective than antisense CK2-beta in most of the cells tested. The efficacy of the antisense ODN seemed to vary with the cell type; howeve r, in all cases potent induction of apoptosis was observed. Significantly, the effects of the antisense ODN on the CK2 activity in the nuclear matrix were relatively small compared to the much stronger induction of apoptosis in cells. This suggests that modest down-regulation of CK2 can evoke a much greater apoptotic response in cancer cells.