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Protein kinase C delta overexpression enhances radiation sensitivity via extracellular regulated protein kinase 1/2 activation, abolishing the radiation-induced G(2)-M arrest
- Protein kinase C delta overexpression enhances radiation sensitivity via extracellular regulated protein kinase 1/2 activation, abolishing the radiation-induced G(2)-M arrest
- Lee, YJ; Soh, JW; Dean, NM; Cho, CK; Kim, TH; Lee, SJ; Lee, YS
- Ewha Authors
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- Journal Title
- CELL GROWTH & DIFFERENTIATION
- vol. 13, no. 5, pp. 237 - 246
- AMER ASSOC CANCER RESEARCH
- Protein kinase C (PKC) has been widely implicated in regulation of cell growth/cell cycle progression and apoptosis. However, the role of PKCS in radiosensitivity and cell cycle regulation remains unclear. Overexpression of PKCdelta increased Ca2+- independent PKC activity without altering other PKC isoforms (PKCalpha, -beta1, -epsilon, and -zeta), and extracellular regulated protein kinase (ERK) 1/2 activity was also increased in PKCdelta-specific manner. A clonogenic survival assay showed that PKCdelta-overexpressed cells had more radiosensitivity and pronounced induction of apoptosis than control cells. Flow cytometric analysis revealed that PKCdelta made the cells escape from radiation-induced G(2)-M arrest. Moreover, p53 and p21(Waf) induction by radiation were higher in PKCdelta-overexpressed cells than control cells, and PKCdelta-mediated apoptosis was reduced, when radiation-induced ERK1/2 activity was inhibited by PD98059. Furthermore, PKCdelta antisense and rottlerin, PKC inhibitor-abrogated PKCS-mediated radiosensitivity and reduced ERK1/2 activity to the control vector level. These results demonstrated that PKCS overexpression enhanced radiation-induced apoptosis and radiosensitivity via ERK1/2 activation, thereby abolishing the radiation-induced G(2)-M arrest and finally apoptosis.
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