NDLI: PROTEASOME INHIBITION BY BORTEZOMIB INCREASES IL-8 EXPRESSION IN ANDROGEN-INDEPENDENT PROSTATE CANCER CELLS: THE ROLE OF $IKKα^{}$

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Plasma B lymphocyte stimulator and B cell differentiation in idiopathic pulmonary fibrosis patients.

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PROTEASOME INHIBITION BY BORTEZOMIB INCREASES IL-8 EXPRESSION IN ANDROGEN-INDEPENDENT PROSTATE CANCER CELLS: THE ROLE OF $IKKα^{}$

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PROTEASOME INHIBITION BY BORTEZOMIB INCREASES IL-8 EXPRESSION IN ANDROGEN-INDEPENDENT PROSTATE CANCER CELLS: THE ROLE OF $IKKα^{}$

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Phyo, Sai Aung Manna, Subrata Vancurova, Ivana Gatla, Himavanth Reddy Singha, Bipradeb Ramaswami, Sitharam Chang, Tzu-Pei Sanacora, Shannon
Description	Country affiliation: United States Author Affiliation: Manna S ( Department of Biological Sciences, St. John's University, New York, NY 11439, USA.)
Abstract	Expression of the proinflammatory and proangiogenic chemokine IL-8, which is regulated at the transcriptional level by NF-κB, is constitutively increased in androgen-independent metastatic prostate cancer and correlates with poor prognosis. Inhibition of NF-κB-dependent transcription was used as an anticancer strategy for the development of the first clinically approved 26S proteasome inhibitor, bortezomib (BZ). Even though BZ has shown remarkable antitumor activity in hematological malignancies, it has been less effective in prostate cancer and other solid tumors; however, the mechanisms have not been fully understood. In this article, we report that proteasome inhibition by BZ unexpectedly increases IL-8 expression in androgen-independent prostate cancer PC3 and DU145 cells, whereas expression of other NF-κB-regulated genes is inhibited or unchanged. The BZ-increased IL-8 expression is associated with increased in vitro p65 NF-κB DNA binding activity and p65 recruitment to the endogenous IL-8 promoter. In addition, proteasome inhibition induces a nuclear accumulation of IκB kinase (IKK) , and inhibition of IKK enzymatic activity significantly attenuates the BZ-induced p65 recruitment to IL-8 promoter and IL-8 expression, demonstrating that the induced IL-8 expression is mediated, at least partly, by IKK . Together, these data provide the first evidence, to our knowledge, for the gene-specific increase of IL-8 expression by proteasome inhibition in prostate cancer cells and suggest that targeting both IKK and the proteasome may increase BZ effectiveness in treatment of androgen-independent prostate cancer.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1300895
Journal	The Journal of Immunology
Issue Number	5
Volume Number	191
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-09-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antineoplastic Agents Pharmacology Boronic Acids I-kappa B Kinase Metabolism Interleukin-8 Biosynthesis Prostatic Neoplasms Proteasome Endopeptidase Complex Drug Effects Pyrazines Blotting, Western Bortezomib Cell Line, Tumor Chromatin Immunoprecipitation Enzyme-linked Immunosorbent Assay Rna, Small Interfering Real-time Polymerase Chain Reaction Transfection Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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