title: Bcl-3 suppresses Tax-induced NF-κB activation through p65 nuclear translocation             blockage in HTLV-1-infected cells.
abstract: Human T cell leukemia virus type 1 (HTLV-1) Tax-induced persistent activation             of the NF-κB pathway is perceived as the primary cause of adult T cell leukemia             (ATL), an aggressive leukemia caused by HTLV-1. Although elevated oncoprotein             Bcl-3 levels are found in many HTLV-1-infected T cell lines and ATL cells, the             role of Bcl-3 in the malignant progression caused by HTLV-1 retrovirus remains             poorly understood. We confirmed, in the present study, that the Tax-induced NF-κB             activation involves the regulation of Bcl-3. Both knockdown and overexpression             of Bcl-3 inhibit the Tax-induced NF-κB activation. Similarly, excessive Bcl-3             inhibits the NF-κB/DNA binding activity and significantly decreases Tax-induced             p65 nuclear translocation. The present results demonstrate the pleiotropic roles             of Bcl-3 in Tax-induced NF-κB activation and indicate that a balance in the aberrant             Bcl-3 expression may be established to play an important role in the maintenance             of proliferation and inhibition of apoptosis in HTLV-1-infected and ATL cells.
authors.affiliation: Research Center for Immunology, Xinxiang Medical University, Xinxiang, Henan, People's Republic of China.
authors.forename: Jinheng
authors.initials: J
authors.lastname: Wang
authors.forename: Junying
authors.initials: J
authors.lastname: Li
authors.forename: Yanmei
authors.initials: Y
authors.lastname: Huang
authors.forename: Xiangfeng
authors.initials: X
authors.lastname: Song
authors.forename: Zhiguo
authors.initials: Z
authors.lastname: Niu
authors.forename: Zhitao
authors.initials: Z
authors.lastname: Gao
authors.forename: Hui
authors.initials: H
authors.lastname: Wang
mesh_terms: D000328:Adult; D017209:Apoptosis; D000081242:B-Cell Lymphoma 3 Protein; D015153:Blotting, Western; D002467:Cell Nucleus / Q000187:drug effects / Q000378:metabolism; D049109:Cell Proliferation; D003593:Cytoplasm / Q000187:drug effects / Q000378:metabolism; D024202:Electrophoretic Mobility Shift Assay; D005455:Fluorescent Antibody Technique; D016356:Gene Products, tax / Q000494:pharmacology*; D015368:Human T-lymphotropic virus 1 / Q000472:pathogenicity; D006801:Humans; D015459:Leukemia-Lymphoma, Adult T-Cell / Q000235:genetics / Q000378:metabolism / Q000517:prevention & control*; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D009570:Nitriles / Q000494:pharmacology; D010957:Plasmids / Q000235:genetics; D021381:Protein Transport; D011518:Proto-Oncogene Proteins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D034741:RNA, Small Interfering / Q000235:genetics; D013450:Sulfones / Q000494:pharmacology; D051996:Transcription Factor RelA / Q000378:metabolism*; D014157:Transcription Factors / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D014407:Tumor Cells, Cultured
chemical_list: C434003:3-(4-methylphenylsulfonyl)-2-propenenitrile; D000081242:B-Cell Lymphoma 3 Protein; C000631344:BCL3 protein, human; D016356:Gene Products, tax; D016328:NF-kappa B; D009570:Nitriles; D011518:Proto-Oncogene Proteins; D034741:RNA, Small Interfering; D013450:Sulfones; D051996:Transcription Factor RelA; D014157:Transcription Factors