Related Experiment Video
Updated: May 11, 2026

In situ Subcellular Fractionation of Adherent and Non-adherent Mammalian Cells
Published on: July 23, 2010
Biochemical and functional interactions of human papillomavirus proteins with polycomb group proteins
Margaret E McLaughlin-Drubin1, Karl Munger
1Division of Infectious Diseases, Brigham and Women's Hospital and Department of Medicine, Harvard Medical School, 181 Longwood Avenue, MCP 861, Boston, MA 02115, USA. mdrubin@rics.bwh.harvard.edu
Abstract:
The role of enzymes involved in polycomb repression of gene transcription has been studied extensively in human cancer. Polycomb repressive complexes mediate oncogene-induced senescence, a principal innate cell-intrinsic tumor suppressor pathway that thwarts expansion of cells that have suffered oncogenic hits. Infections with human cancer viruses including human papillomaviruses (HPVs) and Epstein-Barr virus can trigger oncogene-induced senescence, and the viruses have evolved strategies to abrogate this response in order to establish an infection and reprogram their host cells to establish a long-term persistent infection. As a consequence of inhibiting polycomb repression and evading oncogene induced-senescence, HPV infected cells have an altered epigenetic program as evidenced by aberrant homeobox gene expression. Similar alterations are frequently observed in non-virus associated human cancers and may be harnessed for diagnosis and therapy.
Insights
Polycomb repression pathways are crucial for suppressing cancer by halting cell growth. Human papillomaviruses (HPVs) evade this, altering gene expression and potentially aiding cancer development.
Area of Science:
- Molecular Biology
- Epigenetics
- Cancer Research
Background:
- Polycomb repressive complexes are key regulators of gene transcription and act as tumor suppressors via oncogene-induced senescence.
- Viruses like human papillomaviruses (HPVs) can disrupt this senescence pathway to establish persistent infections.
- Disruption of polycomb repression and evasion of senescence lead to altered epigenetic programs, including aberrant homeobox gene expression.
Purpose of the Study:
- To investigate the role of enzymes in polycomb repression in human cancer.
- To understand how viral infections, specifically HPVs, interfere with oncogene-induced senescence.
- To explore the implications of altered epigenetic programs in virus-associated and non-virus-associated cancers.
Main Methods:
- Review of existing literature on polycomb repression in human cancer.
- Analysis of mechanisms by which human cancer viruses abrogate oncogene-induced senescence.
- Examination of epigenetic alterations, specifically homeobox gene expression, in HPV-infected cells and other human cancers.
Main Results:
- Polycomb repressive complexes are vital for innate tumor suppression through oncogene-induced senescence.
- Human cancer viruses, including HPVs, possess strategies to inhibit polycomb repression and evade senescence.
- HPV infection results in altered epigenetic programs, characterized by aberrant homeobox gene expression, mirroring changes seen in other human cancers.
Conclusions:
- Inhibition of polycomb repression and evasion of oncogene-induced senescence by viruses like HPV contribute to cancer development.
- Aberrant homeobox gene expression in HPV-infected cells represents a significant epigenetic alteration.
- These viral-induced epigenetic changes are relevant to non-virus-associated human cancers and hold potential for diagnostic and therapeutic applications.
Related Concept Videos
Abnormal Proliferation
Covalently Linked Protein Regulators
These groups modify specific amino acids in a protein.
Mechanisms of Retrovirus-induced Cancers
Mechanisms of Retrovirus-induced Cancers
Position-effect Variegation
Combinatorial Gene Control
The expression of more than 30,000 genes is controlled by approximately 2000-3000 transcription factors. This is possible because a single transcription factor can recognize more than one regulatory sequence. The specificity in gene...

