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IKBKE is over-expressed in glioma and contributes to resistance of glioma cells to apoptosis via activating NF-κB

Guan, Hongyu ; Zhang, Heng ; Cai, Junchao ; Wu, Jueheng ; Yuan, Jie ; Li, Jun ; Huang, Zhengsong ; Li, Mengfeng

The Journal of pathology, 2011-02, Vol.223 (3), p.436-445 [Periódico revisado por pares]

Chichester, UK: John Wiley & Sons, Ltd

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IKBKE is over-expressed in glioma and contributes to resistance of glioma cells to apoptosis via activating NF-κB
Autor: Guan, Hongyu ; Zhang, Heng ; Cai, Junchao ; Wu, Jueheng ; Yuan, Jie ; Li, Jun ; Huang, Zhengsong ; Li, Mengfeng
Assuntos: Adult ; Antibiotics, Antineoplastic - pharmacology ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - physiology ; Apoptosis - radiation effects ; Bcl-2 protein ; Biological and medical sciences ; Brain tumors ; Breast cancer ; Data processing ; Doxorubicin - pharmacology ; Female ; Gene Expression Regulation, Enzymologic ; Glioma ; Glioma - enzymology ; Glioma - pathology ; Glioma cells ; Humans ; I Kappa B kinase ; I-kappa B Kinase - genetics ; I-kappa B Kinase - metabolism ; IKBKE ; IKK protein ; Immunohistochemistry ; Investigative techniques, diagnostic techniques (general aspects) ; Male ; Medical sciences ; Middle Aged ; mRNA ; Neurology ; NF- Kappa B protein ; NF-kappa B - physiology ; NF-κB ; Ovarian cancer ; Overexpression ; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques ; Prostate cancer ; Reverse Transcriptase Polymerase Chain Reaction - methods ; RNA, Messenger - genetics ; RNA, Neoplasm - genetics ; Signal Transduction - drug effects ; Tumor Cells, Cultured ; Tumors of the nervous system. Phacomatoses ; U.V. radiation ; Ultraviolet Rays ; Up-Regulation
É parte de: The Journal of pathology, 2011-02, Vol.223 (3), p.436-445
Notas: Science and Technology Department of Zhuhai Municipality, Guangdong Province, China - No. PC20071076
National High-Tech R&D Programme - No. 2006AA02A223; No. 2007AA09Z448
Key Science and Technique Research Project of Guangdong Province - No. 2007A03260001; No. 2009A 020101006; No. 2009B020600001; No. 2010B0306-00003
ArticleID:PATH2815
Ministry of Science and Technology of China - No. 973)2005CB724-605
Guangdong Provincial Natural Science Foundation - No. 8151008901000014; No. 06201946
National Science and Technique Major Project - No. 2009ZX09103-04; No. 201005022; No. 2009ZX10004-213
Natural Science Foundation of China - No. 30872930; No. U0632002; No. 81001121; No. 40806059
No conflicts of interest were declared.
istex:E6C885CC915085718D6A7EE106A6FFA5CF4B7C8D
ark:/67375/WNG-T2CVL8R3-R
These authors contributed equally to this study.
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Descrição: IκB kinase‐ε (IKBKE), a member of the IκB kinase (IKK) family, has been identified as an oncogenic protein and found to be up‐regulated in breast cancer, ovarian cancer and prostate cancer. Nonetheless, the expression status and functional significance of IKBKE in human glioma remain unexplored. For the first time, we have demonstrated that mRNA and protein levels of IKBKE were robustly up‐regulated in glioma cell lines and human primary glioma tissues. Immunohistochemistry analysis revealed that 53.5% (38/71) paraffin‐embedded archived glioma specimens exhibited high levels of IKBKE expression. Intriguingly, there was no significant difference in IKBKE expression among different grades of glioma. To understand the biological function of IKBKE in the development and progression of human glioma, glioma cells lines ectopically over‐expressing IKBKE were established and tested for their responsiveness to apoptotic inducers. Our data showed that IKBKE over‐expression inhibited cell apoptosis induced by UV irradiation or adriamycin and, in contrast, shRNAi‐mediated suppression of IKBKE increased the sensitivity of glioma cells to the apoptotic inducers. Importantly, we found that up‐regulated IKBKE could induce the expression of Bcl‐2 through activating NF‐κB signalling, and that, specifically, we identified IκB as a critical component for this signalling cascade. The current study suggests that up‐regulation of IKBKE may represent an important molecular hallmark that is biologically and clinically relevant to the development and progression, as well as the chemo‐ and radio‐resistance, of the disease. Copyright © 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Editor: Chichester, UK: John Wiley & Sons, Ltd
Idioma: Inglês

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IKBKE is over-expressed in glioma and contributes to resistance of glioma cells to apoptosis via activating NF-κB

Guan, Hongyu ; Zhang, Heng ; Cai, Junchao ; Wu, Jueheng ; Yuan, Jie ; Li, Jun ; Huang, Zhengsong ; Li, Mengfeng

Chichester, UK: John Wiley & Sons, Ltd

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