REGULATION OF IAPs GENE FAMILY BY INTERLEUKIN-1α AND EPSTEIN-BARR VIRUS IN NASOPHARYNGEAL CARCINOMA

被引:4
作者
Chua, Huey-Huey [1 ]
Yeh, Te-Huei [2 ]
Wang, Ying-Piao [3 ,4 ]
Sheen, Tzung-Shiahn [2 ]
Shew, Jin-Yuh [5 ]
Huang, Yu-Tzu [1 ]
Tsai, Ching-Hwa [1 ]
机构
[1] Natl Taiwan Univ, Grad Inst Microbiol, Coll Med, Sect 1, Taipei 10051, Taiwan
[2] Natl Taiwan Univ, Natl Taiwan Univ Hosp, Coll Med, Dept Otolaryngol, Taipei 10051, Taiwan
[3] Mackay Mem Hosp, Dept Otolaryngol, Taipei, Taiwan
[4] Mackay Med Nursing & Management Coll, Taipei, Taiwan
[5] Natl Taiwan Univ, Grad Inst Biochem & Mol Biol, Coll Med, Taipei 10051, Taiwan
来源
HEAD AND NECK-JOURNAL FOR THE SCIENCES AND SPECIALTIES OF THE HEAD AND NECK | 2008年 / 30卷 / 12期
关键词
nasopharyngeal carcinoma; Epstein-Barr virus; apoptosis; inhibitor of apoptosis protein; interleukin-1; alpha;
D O I
10.1002/hed.20896
中图分类号
R76 [耳鼻咽喉科学];
学科分类号
100213 ;
摘要
Background. Inhibitors of apoptosis proteins (IAPs), which counteract apoptosis by potently inhibiting caspase activation, are promising targets of new anti-tumor therapy. However, their roles in the pathogenesis of nasopharyngeal carcinoma (NPC), an Epstein-Barr virus (EBV)-associated carcinoma, are not fully understood. Herein, we investigated the expression and regulation of IAPs in NPC. Methods and Results. Using real-time quantitative polymerase chain reaction (PCR) analysis, we found that among the IAPs family only the transcription of survivin, HIAP-1, and HIAP-2 was consistently up-regulated in NPC and metastatic NPC tissues. Immunohistochemical staining showed that their proteins were more predominantly expressed in tumor cells nests, Noteworthy, these IAPs were upregulated by interieukin-1 alpha stimulation or EBV infection, and subsequently resulted in triggering rapid proliferation of NPC verified by strong Ki-67 staining. Conclusion. Survivin, HIAP-1, and HIAP-2 were distinctly upregulated in NPC, suggesting they may play significant roles in NPC tumorigenesis and serve as tumor markers with prognostic and therapeutic implications. (C) 2008 Wiley Periodicals, Inc. Head Neck 30: 1575-1585, 2008
引用
收藏
页码:1575 / 1585
页数:11
相关论文
共 52 条
[1]   A novel anti-apoptosis gene, survivin, expressed in cancer and lymphoma [J].
Ambrosini, G ;
Adida, C ;
Altieri, DC .
NATURE MEDICINE, 1997, 3 (08) :917-921
[2]   Survivin as a radioresistance factor in pancreatic cancer [J].
Asanuma, K ;
Moriai, R ;
Yajima, T ;
Yagihashi, A ;
Yamada, M ;
Kobayashi, D ;
Watanabe, N .
JAPANESE JOURNAL OF CANCER RESEARCH, 2000, 91 (11) :1204-1209
[3]   A small molecule Smac-mimic compound induces apoptosis and sensitizes TRAIL- and etoposide-induced apoptosis in breast cancer cells [J].
Bockbrader, KM ;
Tan, MJ ;
Sun, Y .
ONCOGENE, 2005, 24 (49) :7381-7388
[4]   Cytokine-regulated expression of survivin in myeloid leukemia [J].
Carter, BZ ;
Milella, M ;
Altieri, DC ;
Andreeff, M .
BLOOD, 2001, 97 (09) :2784-2790
[5]   Requirement for cell-to-cell contact in Epstein-Barr virus infection of nasopharyngeal carcinoma cells and keratinocytes [J].
Chang, Y ;
Tung, CH ;
Huang, YT ;
Lu, J ;
Chen, JY ;
Tsai, CH .
JOURNAL OF VIROLOGY, 1999, 73 (10) :8857-8866
[6]   Upregulation of discoidin domain receptor 2 in nasopharyngeal carcinoma [J].
Chua, Huey-Huey ;
Yeh, Te-Huei ;
Wang, Ying-Piao ;
Huang, Yu-Tzu ;
Sheen, Tzung-Shiahn ;
Lo, You-Chang ;
Chou, Ya-Ching ;
Tsai, Ching-Hwa .
HEAD AND NECK-JOURNAL FOR THE SCIENCES AND SPECIALTIES OF THE HEAD AND NECK, 2008, 30 (04) :427-436
[7]  
Codd JD, 1999, J PATHOL, V187, P549
[8]   Epstein-Barr virus latent membrane protein 1 (LMP1) activates the phosphatidylinositol 3-kinase/Akt pathway to promote cell survival and induce actin filament remodeling [J].
Dawson, CW ;
Tramountanis, G ;
Eliopoulos, AG ;
Young, LS .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (06) :3694-3704
[9]   IAPs block apoptotic events induced by caspase-8 and cytochrome c by direct inhibition of distinct caspases [J].
Deveraux, QL ;
Roy, N ;
Stennicke, HR ;
Van Arsdale, T ;
Zhou, Q ;
Srinivasula, SM ;
Alnemri, ES ;
Salvesen, GS ;
Reed, JC .
EMBO JOURNAL, 1998, 17 (08) :2215-2223
[10]   Smac, a mitochondrial protein that promotes cytochrome c-dependent caspase activation by eliminating IAP inhibition [J].
Du, CY ;
Fang, M ;
Li, YC ;
Li, L ;
Wang, XD .
CELL, 2000, 102 (01) :33-42