RPAP3 enhances cytotoxicity of doxorubicin by impairing NF-kappa B pathway
- Department of Pharmacology, Graduate School of Dentistry, Osaka University, Suita, Osaka (Japan)
- Department of Fixed Prosthodontics, Osaka University (Japan)
- Department of Oral and Maxillofacial Surgery II, Osaka University (Japan)
- Department of Biophysics and Biochemistry, Graduate School of Medicine and Cell Biology and Metabolism Group, Graduate School of Frontier Biosciences, Osaka University (Japan)
Research highlights: {yields} RNA polymerase II-associated protein 3 (RPAP3) possesses an activity to bind with NEMO and to inhibit the ubiquitination of NEMO. {yields} RPAP3 enhances doxorubicin-induced cell death in breast cancer cell line T-47D through the marked impairment of NF-{kappa}B pathway. {yields} RPAP3 is a novel modulator of NF-{kappa}B pathway in apoptosis induced by anti-cancer chemotherapeutic agents. -- Abstract: Activation of anti-apoptotic gene transcription by NF-{kappa}B (nuclear factor-kappa B) has been reported to be linked with a resistance of cancer cells against chemotherapy. NEMO (NF-{kappa}B essential modulator) interacts with a number of proteins and modulates the activity of NF-{kappa}B pathway. In this study, we revealed that RPAP3 (RNA polymerase II-associated protein 3) possesses an activity to bind with NEMO and to inhibit the ubiquitination of NEMO and that RPAP3 enhances doxorubicin-induced cell death in breast cancer cell line T-47D through the marked impairment of NF-{kappa}B pathway. These results indicate that RPAP3 may be a novel modulator of NF-{kappa}B pathway in apoptosis induced by anti-cancer chemotherapeutic agents.
- OSTI ID:
- 22204767
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 404, Issue 4; Other Information: Copyright (c) 2010 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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