Literature DB >> 25503124

Inhibition of P-TEFb by DRB suppresses SIRT1/CK2α pathway and enhances radiosensitivity of human cancer cells.

Zhi-Qiang Wang1, Casey L Johnson1, Amit Kumar1, David P Molkentine1, Jessica M Molkentine1, Tatiana Rabin1, Kathryn A Mason1, Luka Milas1, Uma Raju2.   

Abstract

BACKGROUND: Positive transcription elongation factor-b (P-TEFb) is a complex containing CDK9 and a cyclin (T1, T2 or K). The effect of inhibition of P-TEFb by 5,6-dichloro-l-β-D-ribofuranosyl benzimidazole (DRB) on cell radiosensitivity and the underlying mechanisms were investigated.
MATERIALS AND METHODS: Six human cancer cell lines were subjected to (3)H-uridine incorporation, cell viability and clonogenic cell survival assays; cell-cycle redistribution and apoptosis assay; western blots and nuclear 53BP1 foci analysis after exposing the cells to DRB with/without γ-radiation.
RESULTS: DRB suppressed colony formation and enhanced radiosensitivity of all cell lines. DRB caused a further increase in radiation-induced apoptosis and cell-cycle redistribution depending on p53 status. DRB prolonged the presence of radiation-induced nuclear p53 binding protein-1 (53BP1) foci and suppressed the expression of sirtuin-1 (SIRT1) and casein kinase 2-alpha (CK2α), suggesting an inhibition of DNA repair processes.
CONCLUSION: Our findings indicate that DRB has the potential to increase the efficacy of radiotherapy and warrants further investigation using in vivo tumor models. Copyright
© 2014 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved.

Entities:  

Keywords:  CDK9; CK2α; DNA repair; DRB; RNA polymerase II; SIRT1; radiosensitivity

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Year:  2014        PMID: 25503124

Source DB:  PubMed          Journal:  Anticancer Res        ISSN: 0250-7005            Impact factor:   2.480


  4 in total

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  4 in total

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