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

Nurshamimi Nor Rashid1, Rohana Yusof2, Roger J Watson3

  • 1Section 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.

Anticancer Research
|November 5, 2014
PubMed
Abstract

Insights

The B-myb-DREAM complex is not essential for cell cycle progression in human papillomavirus (HPV)-infected cells lacking a G1/S checkpoint. Its role in viral replication is less critical than the p130-DREAM complex.

Area of Science:

  • Molecular biology
  • Cell cycle regulation
  • Virology

Background:

  • Human papillomavirus (HPV) E7 proteins disrupt retinoblastoma (RB) protein interactions, affecting E2F transcription factors.
  • Previous studies indicated HPV16 E7 disrupts the repressive p130-DREAM complex for viral replication.
  • Increased B-myb-DREAM complex expression was observed in HPV-transformed cells.

Purpose of the Study:

  • To investigate the role of the activator B-myb-DREAM complex in HPV-induced replication and mitosis.
  • To determine if the B-myb-DREAM complex is critical for cell cycle progression in HPV-transformed cells.

Main Methods:

  • Depletion of LIN-54 and B-myb in HPV-transformed cell lines (CaSki, SiHa, T98G).
  • Flow cytometry analysis to assess cell cycle distribution.
  • Quantitative PCR to measure mRNA levels of S/G2 phase genes.

Main Results:

  • Depletion of LIN-54 decreased B-myb association with LIN-54 and LIN-9.
  • LIN-54 depletion led to an increased proportion of G2/M phase cells.
  • Depletion of B-myb mirrored the effects of LIN-54/LIN-9 depletion on cell cycle and S/G2 gene expression.

Conclusions:

  • The B-myb-DREAM complex may not be vital for mitosis progression in cells lacking a G1/S checkpoint.
  • The B-myb-DREAM complex is less critical for HPV survival compared to the p130-DREAM complex.

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