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The inner nuclear membrane protein, Banf1, has an essential role in triple negative breast cancer cell proliferation

Maddison Rose1, Joshua T Burgess1, Chee Man Cheong1

  • 1Cancer Genomics Program, Centre for Genomics and Personalised Health, School of Biomedical Sciences, Faculty of Health, Queensland University of Technology, Kelvin Grove, Brisbane, Australia.

Scientific Reports
|July 15, 2025
PubMed

Insights

Triple negative breast cancer (TNBC) cells show significant Barrier-to-Autointegration Factor 1 (Banf1) overexpression. Targeting Banf1 inhibits TNBC proliferation and induces cell death, suggesting its potential as a novel therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Triple negative breast cancer (TNBC) presents poor survival outcomes and limited targeted therapies.
  • Current treatment relies on conventional chemotherapy, necessitating novel therapeutic strategies.

Purpose of the Study:

  • To investigate the therapeutic potential of Barrier-to-Autointegration Factor 1 (Banf1) as a novel target in TNBC.
  • To determine Banf1 expression and localization in breast cells and TNBC cell lines.

Main Methods:

  • Bioinformatic analysis of patient samples for Banf1 expression across breast cancer subtypes and stages.
  • Experimental validation of Banf1's role in TNBC cell proliferation, cell cycle, and cell death.

Main Results:

  • Banf1 is significantly overexpressed in all stages and subtypes of breast cancer.
  • Banf1 depletion in TNBC cells led to inhibited proliferation and mitotic arrest.
  • Loss of nuclear envelope integrity and aberrant nuclear morphology were observed upon Banf1 depletion, inducing TNBC-specific cell death.

Conclusions:

  • Banf1 is overexpressed and functionally involved in TNBC progression.
  • Banf1 represents a promising novel therapeutic target for TNBC treatment.
  • Further research into Banf1-targeted therapies for TNBC is warranted.
Keywords:
Banf1Breast cancerMitosisNuclear envelope

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