Examination of CK2α and NF-κB p65 expression in human benign prostatic hyperplasia and prostate cancer tissues.
Examination of CK2α and NF-κB p65 expression in human benign prostatic hyperplasia and prostate cancer tissues.
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DOI：
10.1007/s11010-016-2765-3
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发表时间：
2016-09
影响因子：
4.3
通讯作者：
Ahmed K
中科院分区：
文献类型：
--
作者：
Qaiser F;Trembley JH;Sadiq S;Muhammad I;Younis R;Hashmi SN;Murtaza B;Rector TS;Naveed AK;Ahmed K
Protein kinase CK2 plays a critical role in cell growth, proliferation, and suppression of cell death. CK2 is overexpressed, especially in the nuclear compartment, in the majority of cancers, including prostate cancer (PCa). CK2-mediated activation of transcription factor nuclear factor kappa B (NF-κB) p65 is a key step in cellular proliferation, resulting in translocation of NF-κB p65 from the cytoplasm to the nucleus. As CK2 expression and activity are also elevated in benign prostatic hyperplasia (BPH), we sought to increase the knowledge of CK2 function in benign and malignant prostate by examination of the relationships between nuclear CK2 and nuclear NF-κB p65 protein expression. The expression level and localization of CK2α and NF-κB p65 proteins in PCa and BPH tissue specimens was determined. Nuclear CK2α and NF-κB p65 protein levels are significantly higher in PCa compared with BPH, and these proteins are positively correlated with each other in both diseases. Nuclear NF-κB p65 levels correlated with Ki-67 or with cytoplasmic NF-κB p65 expression in BPH, but not in PCa. The findings provide information that combined analysis of CK2α and NF-κB p65 expression in prostate specimens relates to the disease status. Increased nuclear NF-κB p65 expression levels in PCa specifically related to nuclear CK2α levels, indicating a possible CK2-dependent relationship in malignancy. In contrast, nuclear NF-κB p65 protein levels related to both Ki-67 and cytoplasmic NF-κB p65 levels exclusively in BPH, suggesting a potential separate impact for NF-κB p65 function in proliferation for benign disease as opposed to malignant disease.
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影响因子：
7.3
作者：
Gao J;Aksoy BA;Dogrusoz U;Dresdner G;Gross B;Sumer SO;Sun Y;Jacobsen A;Sinha R;Larsson E;Cerami E;Sander C;Schultz N
通讯作者：
Schultz N
影响因子：
2.8
作者：
Lin-Tsai, Opal;Clark, Peter E.;Miller, Nicole L.;Fowke, Jay H.;Hameed, Omar;Hayward, Simon W.;Strand, Douglas W.
通讯作者：
Strand, Douglas W.
影响因子：
3.7
作者：
Guo Z;Xing Z;Cheng X;Fang Z;Jiang C;Su J;Zhou Z;Xu Z;Holmberg A;Nilsson S;Liu Z
通讯作者：
Liu Z
影响因子：
64.5
作者：
Cancer Genome Atlas Research Network
通讯作者：
Cancer Genome Atlas Research Network
影响因子：
8
作者：
Dominguez, I.;Sonenshein, G. E.;Seldin, D. C.
通讯作者：
Seldin, D. C.