Am J Cancer Res 2013;3(5):433-445
Review Article
NFκB function and regulation in cutaneous T-cell lymphoma
Tzu-Pei Chang, Ivana Vancurova
Department of Biological Sciences, St. John’s University, New York, NY 11439, USA
Received August 1, 2013; Accepted August 23, 2013; Epub November 1, 2013; Published November 15, 2013
Abstract: The nuclear accumulation and transcriptional activity of NFκB are constitutively increased in cutaneous T-cell
lymphoma (CTCL) cells, and are responsible for their increased survival and proliferation. However, in addition to the anti-
apoptotic and pro-inflammatory genes, NFκB induces expression of immunosuppressive genes, such as IL-10 and TGFβ, which
inhibit the immune responses and are characteristic for the advanced stages of CTCL. While the mechanisms regulating NFκB-
dependent transcription of anti-apoptotic and pro-inflammatory genes have been studied extensively, very little is known about
the NFκB regulation of immunosuppressive genes. The specificity of NFκB-regulated responses is determined by the subunit
composition of NFκB complexes recruited to the individual promoters, post-translational modifications of NFκB proteins, as well
as by their interactions with other transcriptional factors and regulators. In this review, we discuss the mechanisms regulating
the transcription of NFκB-dependent anti-apoptotic, pro-inflammatory and immunosuppressive genes in CTCL cells, as potential
targets for CTCL therapies. (ajcr0000222).
Keywords: Apoptosis, bortezomib, cutaneous T cell lymphoma, IκBα, IL-10, immunosuppression, NFκB, proteasome inhibition,
TGFβ
Address correspondence to: Dr. Ivana Vancurova, Department of Biological Sciences, St. John’s University, 8000 Utopia
Parkway, Queens, NY 11439. Tel: 718-990-6409; E-mail: vancuroi@stjohns.edu
Review Article
NFκB function and regulation in cutaneous T-cell lymphoma
Tzu-Pei Chang, Ivana Vancurova
Department of Biological Sciences, St. John’s University, New York, NY 11439, USA
Received August 1, 2013; Accepted August 23, 2013; Epub November 1, 2013; Published November 15, 2013
Abstract: The nuclear accumulation and transcriptional activity of NFκB are constitutively increased in cutaneous T-cell
lymphoma (CTCL) cells, and are responsible for their increased survival and proliferation. However, in addition to the anti-
apoptotic and pro-inflammatory genes, NFκB induces expression of immunosuppressive genes, such as IL-10 and TGFβ, which
inhibit the immune responses and are characteristic for the advanced stages of CTCL. While the mechanisms regulating NFκB-
dependent transcription of anti-apoptotic and pro-inflammatory genes have been studied extensively, very little is known about
the NFκB regulation of immunosuppressive genes. The specificity of NFκB-regulated responses is determined by the subunit
composition of NFκB complexes recruited to the individual promoters, post-translational modifications of NFκB proteins, as well
as by their interactions with other transcriptional factors and regulators. In this review, we discuss the mechanisms regulating
the transcription of NFκB-dependent anti-apoptotic, pro-inflammatory and immunosuppressive genes in CTCL cells, as potential
targets for CTCL therapies. (ajcr0000222).
Keywords: Apoptosis, bortezomib, cutaneous T cell lymphoma, IκBα, IL-10, immunosuppression, NFκB, proteasome inhibition,
TGFβ
Address correspondence to: Dr. Ivana Vancurova, Department of Biological Sciences, St. John’s University, 8000 Utopia
Parkway, Queens, NY 11439. Tel: 718-990-6409; E-mail: vancuroi@stjohns.edu
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American Journal of Cancer Research
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