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

## TL;DR

This study identifies Banf1 as a key protein involved in the growth and survival of triple negative breast cancer cells, suggesting it could be a new target for treatment.

## Contribution

The study reveals Banf1's essential role in TNBC progression and its potential as a novel therapeutic target.

## Key findings

- Banf1 is overexpressed in all breast cancer stages and subtypes.
- Banf1 depletion causes mitotic arrest and cell death in TNBC cells.
- Loss of Banf1 disrupts nuclear envelope integrity and nuclear morphology.

## Abstract

Triple negative breast cancers (TNBCs) are a heterogenous subcategory of breast cancers which have significantly worse survival outcomes compared to other breast cancer subtypes. However, limited advances have been made towards a targeted TNBC therapeutic and traditional chemotherapies remain the frontline therapy. Therefore, this study aimed to examine the therapeutic potential of a novel TNBC target, Barrier-to-Autointegration Factor 1 (Banf1), including determining Banf1 expression and cellular localisation in non-malignant breast cells and a panel of TNBC cell lines. Bioinformatic analysis of patient samples demonstrated that Banf1 is overexpressed in all breast cancer stages and subtypes. Banf1 depletion inhibited proliferation and induced mitotic arrest in TNBC cells via loss of nuclear envelope integrity and aberrant nuclear morphology, inducing TNBC tumour cell-specific cell death. These findings highlight the significant overexpression and functional involvement of Banf1 in TNBC progression and suggests that it may have potential as a novel anti-cancer target, supporting further investigation.

The online version contains supplementary material available at 10.1038/s41598-025-10346-x.