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Experimental Therapeutics, Molecular Targets, and Chemical Biology |
1 Department of Radiation Oncology, Case Western Reserve University and 2 Case Comprehensive Cancer Center/University Hospitals of Cleveland, Cleveland, Ohio
Requests for reprints: Timothy J. Kinsella, Department of Radiation Oncology, LTR6068, University Hospitals of Cleveland/Case Comprehensive Cancer Center, 11100 Euclid Avenue, Cleveland, OH 44106-6068. Phone: 216-844-2530; Fax: 216-844-4799; E-mail: timothy.kinsella{at}uhhs.com.
In this study, we show that CK2 (casein kinase II, CKII) participates in apoptotic responses following ionizing radiation (IR). Using HeLa human cervical carcinoma cells, we find that transfection of small interfering RNA against the CK2 
and/or ' catalytic subunits results in enhanced apoptosis following IR damage as measured by flow cytometry techniques, compared with a control small interfering RNA. Within 2 to 6 hours of IR, CK2 partially localizes to perinuclear structures, whereas a marked nuclear localization of ' occurs. Treatment with a pan-caspase inhibitor or transfection of ARC (apoptosis repressor with caspase recruitment domain) suppresses the apoptotic response to IR in the CK2-reduced cells, indicating involvement of caspases. Additionally, we find that CK2 and/or ' reduction affects cell cycle progression independent of IR damage in this human cell line. However, the G2-M checkpoint following IR is not affected in CK2 - and/or '-reduced cells. Thus, our data suggest that CK2 participates in inhibition of apoptosis and negatively regulates caspase activity following IR damage.
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