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Regulation of IAPs gene family by interleukin‐1α and Epstein‐Barr virus in nasopharyngeal carcinoma
Author(s) -
Chua HueyHuey,
Yeh TeHuei,
Wang YingPiao,
Sheen TzungShiahn,
Shew JinYuh,
Huang YuTzu,
Tsai ChingHwa
Publication year - 2008
Publication title -
head and neck
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.012
H-Index - 127
eISSN - 1097-0347
pISSN - 1043-3074
DOI - 10.1002/hed.20896
Subject(s) - nasopharyngeal carcinoma , survivin , carcinogenesis , cancer research , epstein–barr virus , biology , inhibitor of apoptosis , reverse transcription polymerase chain reaction , immunohistochemistry , apoptosis , virus , downregulation and upregulation , immunology , pathology , medicine , gene expression , gene , programmed cell death , radiation therapy , biochemistry
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 interleukin‐1α 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. © 2008 Wiley Periodicals, Inc. Head Neck, 2008