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Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence
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The downregulation of putative anticancer target BORIS/CTCFL in an addicted myeloid cancer cell line modulates the

Evgeny Teplyakov1,2, Qiongfang Wu1, Jian Liu1

  • 1Molecular Epigenetics Laboratory, Guangzhou Institutes of Biomedicine and Health, Guangzhou, China.

Oncotarget
|November 2, 2017
PubMed

Insights

The BORIS/CTCFL gene, a CTCF paralog, is activated in cancer and essential for leukemia cell survival. Downregulating BORIS in K562 cells revealed its role in regulating proliferation and transcription factors.

Area of Science:

  • Epigenetics and Cancer Biology
  • Gene Regulation
  • Chromatin Structure

Background:

  • The BORIS/CTCFL gene is a testis-specific paralog of CTCF, known to be aberrantly activated in various human cancers.
  • While its precise function in cancer is not fully understood, BORIS acts as both a transcription factor and a chromatin architectural protein.
  • BORIS normally functions in germline cells to establish specific gene expression patterns and remodel the epigenetic landscape.

Purpose of the Study:

  • To investigate the downstream pathways regulated by BORIS in cancer cells.
  • To understand the role of BORIS in the self-renewal and survival of cancer cell lines, specifically K562, which are dependent on BORIS.
  • To elucidate the mechanisms by which BORIS influences gene expression and chromatin remodeling in a cancer context.

Main Methods:

  • Downregulation of BORIS expression in the K562 cancer cell line using knockdown techniques.
  • RNA sequencing (RNA-seq) analysis of both mRNA and small non-coding RNAs (including miRNA and piRNA) in BORIS-knockdown cells.
  • Analysis of differentially expressed genes and pathways to identify BORIS-regulated targets.

Main Results:

  • Identification of a set of differentially expressed genes and pathways upon BORIS downregulation, including testis-specific and general proliferation factors.
  • Discovery of key transcriptional regulators, such as SOX6 and LIN28A, among the differentially expressed genes.
  • Evidence suggesting BORIS regulates genes through direct promoter binding and long-distance chromatin domain control.

Conclusions:

  • BORIS activation in leukemia does not merely recapitulate germline functions but establishes a unique regulatory network.
  • BORIS plays a critical role in maintaining the self-renewal and survival of certain cancer cells.
  • The findings highlight BORIS as a potential therapeutic target in cancers where it is aberrantly activated.
Keywords:
CMLCTAchromatinsncRNAtranscriptome

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