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  11. Kdm6a Addiction Of Cervical Carcinoma Cell Lines Is Triggered By E7 And Mediated By P21cip1 Suppression Of Replication Stress

KDM6A addiction of cervical carcinoma cell lines is triggered by E7 and mediated by p21CIP1 suppression of replication stress

David R Soto1, Christopher Barton1, Karl Munger2

  • 1Infectious Diseases Division, Department of Medicine, The Channing Laboratory, Harvard Medical School, Boston, Massachusetts, United States of America.

Plos Pathogens
|October 3, 2017

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View abstract on PubMed

Summary
This summary is machine-generated.

High-risk human papillomavirus (HPV) E7 proteins increase KDM6A, which de-represses p21CIP1. Both are vital for cancer cell survival by managing replication stress.

Area of Science:

  • Oncology
  • Epigenetics
  • Virology

Background:

  • Carcinogenic high-risk human papillomaviruses (HPVs) utilize E7 proteins.
  • E7 protein expression elevates KDM6A (histone demethylase).
  • KDM6A is crucial for high-risk HPV E7-expressing cancer cell survival.

Purpose of the Study:

  • Investigate the role of KDM6A in high-risk HPV E7-expressing cells.
  • Determine the relationship between KDM6A, p21CIP1, and cell survival.
  • Elucidate the mechanism by which KDM6A and p21CIP1 regulate replication stress.

Main Methods:

  • Assessed KDM6A and p21CIP1 expression levels.
  • Depleted KDM6A and p21CIP1 to observe effects on cell viability.
  • Utilized ectopic expression of replication factors and nucleoside supplementation.

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  • Performed DNA damage assays and DNA combing experiments.

    • Main Results:

    • Increased KDM6A epigenetically de-represses p21CIP1 (cell cycle inhibitor).
    • p21CIP1 expression is necessary for high-risk HPV E7-expressing cell survival.
    • p21CIP1 inhibits DNA replication via PCNA binding.
    • Depletion of KDM6A or p21CIP1 leads to replication stress, DNA breaks, and cell death.
    • Nucleoside supplementation rescues viability, indicating replication stress.

    Conclusions:

    • KDM6A and p21CIP1 are essential for managing E7-induced replication stress in high-risk HPV-infected cells.
    • This pathway is critical for the survival of cancer cells expressing high-risk HPV E7.
    • Targeting KDM6A or p21CIP1 may offer therapeutic strategies for HPV-driven cancers.