A B-myb--DREAM complex is not critical to regulate the G2/M genes in HPV-transformed cell lines

Rashid NN 1 , Yusof R 2 , Watson RJ 3

Affiliations 

  • 1 Section of Virology, Department of Medicine, Imperial College London, London, U.K. Department of Molecular Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia nurshamimi@um.edu.my
  • 2 Department of Molecular Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia
  • 3 Section of Virology, Department of Medicine, Imperial College London, London, U.K. Institute of Biomedical Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, U.K
Anticancer Res, 2014 Nov;34(11):6557-63.
PMID: 25368258

Abstract

It is well-established that HPV E7 proteins, encoded by human papillomavirus (HPV) genes, frequently associated with cervical cancers bind avidly to the retinoblastoma (RB) family of pocket proteins and disrupt their association with members of the E2F transcription factor family. Our previous study showed that the repressive p130-dimerization partner, RB-like, E2F and multi-vulval class (DREAM) complex was disrupted by HPV16 E7 proteins in order to maintain the viral replication in CaSki cells. However, we would like to address whether the activator B-myb-DREAM complex is critical in regulating the replication and mitosis phase since our previous study showed increased B-myb-DREAM expression in HPV-transformed cell lines when compared to control cells.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.

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