CPSF6 is a Clinically Relevant Breast Cancer Vulnerability Target: Role of CPSF6 in Breast Cancer

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Updated: Feb 27, 2026

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Najat Binothman1, Ibrahim Y Hachim1, Jean-Jacques Lebrun1

  • 1Department of Medicine, Cancer Research Program, Centre for Translational Biology, McGill University Health Centre, McGill University, Canada.

Ebiomedicine
|July 5, 2017
PubMed

Insights

Cleavage and Polyadenylation Factor-6 (CPSF6) promotes aggressive breast cancer by interacting with RNA editing machinery. Targeting CPSF6 offers a new therapeutic strategy for breast cancer patients with poor prognoses.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Breast cancer remains a significant health concern, with recurrence and progression driving mortality.
  • Aggressive breast cancers often exhibit a loss of cellular differentiation, necessitating the identification of novel therapeutic targets.
  • Understanding the molecular drivers of cancer aggressiveness is crucial for developing effective screening and treatment strategies.

Purpose of the Study:

  • To investigate the role of Cleavage and Polyadenylation Factor-6 (CPSF6) in breast cancer progression and aggressiveness.
  • To identify molecular mechanisms and potential therapeutic targets for aggressive breast cancer subtypes.

Main Methods:

  • Investigated the function of CPSF6 in aggressive breast cancer cell lines (luminal B, HER2-overexpressing, triple-negative).
  • Examined the interaction of CPSF6 with the A-to-I RNA editing machinery, including paraspeckles and the ADAR1 enzyme.
  • Analyzed CPSF6 and paraspeckle protein expression in human breast cancer tissues and correlated with patient outcomes.
  • Assessed the effect of prolactin on CPSF6 and RNA editing activity.

Main Results:

  • CPSF6 is essential for the viability and tumorigenic capacity of aggressive breast cancer cells.
  • CPSF6 physically interacts with and is required for the integrity of the A-to-I RNA editing machinery components, including paraspeckles and ADAR1.
  • CPSF6 and core paraspeckle proteins are overexpressed in human breast cancers, correlating with poor patient outcomes.
  • Prolactin, a mammary differentiation factor, suppresses CPSF6 and RNA editing activity.

Conclusions:

  • CPSF6 plays a novel, tumor-promoting role in aggressive breast cancer.
  • CPSF6 is a potential therapeutic target for improving prognosis and treatment in breast cancer.
  • The interaction between CPSF6 and RNA editing machinery represents a key mechanism in breast cancer aggressiveness.
Keywords:
A-to-I RNA editingDifferentiationLong non-coding RNAMammaryParaspecklesProlactin

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