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Mechanisms of Retrovirus-induced Cancers

Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
Mechanisms of Retrovirus-induced Cancers01:51

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Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
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Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
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Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
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Related Experiment Video

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Testing Cancer Immunotherapeutics in a Humanized Mouse Model Bearing Human Tumors
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BORIS in human cancers -- a review.

Irena Martin-Kleiner1

  • 1Ruder Bošković Institute, Division of Molecular Medicine, P.O. Box 180, 10002 Zagreb, Croatia. kleiner@irb.hr

European Journal of Cancer (Oxford, England : 1990)
|October 25, 2011
PubMed
Summary

Brother of the regulator of the imprinted site (BORIS) is an oncogene implicated in various cancers. Its re-expression in tumors, driven by hypomethylation, correlates with tumor size and grade, suggesting therapeutic potential.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Brother of the regulator of the imprinted site (BORIS), also known as CTCFL, is an 11 zinc finger (ZF) protein and a paralogue of CTCF.
  • BORIS is typically silenced in normal human tissues but re-expressed in various cancers due to promoter hypomethylation.

Purpose of the Study:

  • To investigate the role of BORIS as an oncogene in cancer development and progression.
  • To explore the correlation between BORIS expression levels and clinicopathological features of cancer patients.

Main Methods:

  • Analysis of BORIS expression in different cancer types and normal tissues.
  • Correlation studies between BORIS RNA/protein levels and tumor size/grade.
  • Investigating the effect of DNA methylation inhibitors (e.g., 5-azadC) and histone deacetylase inhibitors on BORIS expression.

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  • Assessing the impact of BORIS silencing on tumor cell apoptosis.
  • Evaluation of BORIS-based antitumor vaccines in preclinical models.

    • Main Results:

    • High BORIS expression correlates with larger tumor size and higher grade in cancer patients.
    • Elevated BORIS transcripts are found in breast, endometrial, prostate, and colon cancers.
    • BORIS expression is induced or enhanced by DNA methylation and histone deacetylase inhibitors.
    • Silencing BORIS induces apoptosis in tumor cell lines.
    • BORIS-based antitumor vaccines show promise in preclinical cancer models.

    Conclusions:

    • BORIS functions as an oncogene, with its aberrant re-expression in cancer linked to disease progression.
    • Epigenetic modifications, particularly hypomethylation, play a crucial role in BORIS activation in tumors.
    • Targeting BORIS, potentially through vaccination strategies, represents a promising avenue for cancer therapy.