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KMID : 0624620120450110659
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BMB Reports
2012 Volume.45 No. 11 p.659 ~ p.664
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IFNγ-mediated inhibition of cell proliferation through increased PKCδ-induced overexpression of EC-SOD
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Jeon Yoon-Jae
Yoo Hyun
Kim Byung-Hak
Lee Yun-Sang
Jeon Byeong-Wook
Kim Sung-Sub
Kim Tae-Yoon
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Abstract
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Extracellular superoxide dismutase (EC-SOD) overexpression modulates cellular responses such as tumor cell suppression and is induced by IFNγ. Therefore, we examined the role of EC-SOD in IFNγ-mediated tumor cell suppression. We observed that the dominant-negative protein kinase C delta (PKCδ) suppresses IFNγ-induced EC-SOD expression in both keratinocytes and melanoma cells. Our results also showed that PKCδ-induced ECSOD expression was reduced by pretreatment with a PKCspecific inhibitor or a siRNA against PKCδ. PKCδ-induced ECSOD expression suppressed cell proliferations by the up-regulation of p21 and Rb, and the downregulation of cyclin A and D. Finally, we demonstrated that increased expression of EC-SOD drastically suppressed lung melanoma proliferation in an EC-SOD transgenic mouse via p21 expression. In summary, our findings suggest that IFNγ-induced EC-SOD expression occurs via activation of PKCδ. Therefore, the upregulation of EC-SOD may be effective for prevention of various cancers, including melanoma, via cell cycle arrest.
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KEYWORD
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EC-SOD, IFNγ, Keratinocytes, Melanoma, PKCδ
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