# BALs are prognostic biomarkers and correlate with malignant behaviors in breast cancer

**Authors:** Xuehao Zhou, Yu Wang, Qingling Xu, Xiang Ao, Mengmeng Chen, Bingqiang Zhang, Ying Liu

PMC · DOI: 10.1186/s12885-025-14576-0 · 2025-07-24

## TL;DR

This study shows that BAL1 and BAL2 proteins are linked to better outcomes in breast cancer and may help predict disease progression.

## Contribution

The study identifies BAL1 and BAL2 as novel prognostic biomarkers and therapeutic targets in breast cancer.

## Key findings

- BAL1 and BAL2 are upregulated in breast cancer and associated with favorable prognosis across multiple subtypes.
- Knockdown of BAL1 and BAL2 reduces cancer cell proliferation and migration while increasing apoptosis.
- BAL1 and BAL2 are proposed as potential therapeutic targets for breast cancer treatment.

## Abstract

The B-aggressive lymphoma (BAL) proteins, including BAL1, BAL2, and BAL3, constitute a conserved protein family characterized by their N-terminal macro domains and putative C-terminal poly (ADP-ribose) polymerase (PARP) active site. Dysregulation of BALs has been closely associated with the progression of various cancers. However, there is limited understanding of their precise expression profile, prognostic significance, and role in breast cancer (BC).

The expression patterns of BALs were evaluated utilizing multiple databases, including Ualcan, Gene Set Cancer Analysis (GSCA), Search Tool for the Retrieval of Interacting Genes/Proteins (STRING), and Gene Expression Profiling Interactive Analysis (GEPIA). The prognostic significance of BALs was assessed via Kaplan-Meier plotter analysis. Furthermore, the potential mechanisms underlying the contribution of BC progression were predicted through GO and KEGG pathway enrichment analysis. Additionally, the effect of BALs on the malignant behaviors of BC cells was determined using CCK-8 assay, Transwell assay, and TUNEL assay.

The data revealed that the expression levels of both BAL1 and BAL2 were upregulated in BC, whereas no significant change was observed for BAL3. Survival analysis demonstrated a strong association between the overexpression of both BAL1 and BAL2 and favorable prognosis in patients with various subtypes of BC, including estrogen receptor (ER)-positive, ER-negative, Basal, luminal B, HER2-, and HER2 + subtypes. Additionally, the knockdown of BAL1 and BAL2 inhibited the proliferation and migration of BC cells while facilitating apoptosis.

These findings suggest that both BAL1 and BAL2 hold great potential as significant prognostic biomarkers and therapeutic targets for patients with BC.

The online version contains supplementary material available at 10.1186/s12885-025-14576-0.

## Linked entities

- **Genes:** PARP9 (poly(ADP-ribose) polymerase family member 9) [NCBI Gene 83666], PARP14 (poly(ADP-ribose) polymerase family member 14) [NCBI Gene 54625], PARP15 (poly(ADP-ribose) polymerase family member 15) [NCBI Gene 165631]
- **Proteins:** PARP9 (poly(ADP-ribose) polymerase family member 9), PARP14 (poly(ADP-ribose) polymerase family member 14), PARP15 (poly(ADP-ribose) polymerase family member 15), PARP1 (poly(ADP-ribose) polymerase 1)
- **Diseases:** breast cancer (MONDO:0004989)

## Full-text entities

- **Genes:** PARP1 (poly(ADP-ribose) polymerase 1) [NCBI Gene 142] {aka ADPRT, ADPRT 1, ADPRT1, ARTD1, PARP, PARP-1}, PARP9 (poly(ADP-ribose) polymerase family member 9) [NCBI Gene 83666] {aka ARTD9, BAL, BAL1, MGC:7868}, ERBB2 (erb-b2 receptor tyrosine kinase 2) [NCBI Gene 2064] {aka CD340, HER-2, HER-2/neu, HER2, MLN 19, MLN-19}, ESR1 (estrogen receptor 1) [NCBI Gene 2099] {aka ER, ESR, ESRA, ESTRR, Era, NR3A1}, PARP15 (poly(ADP-ribose) polymerase family member 15) [NCBI Gene 165631] {aka ARTD7, BAL3, pART7}, PARP14 (poly(ADP-ribose) polymerase family member 14) [NCBI Gene 54625] {aka ARTD8, BAL2, PARP-14, pART8}
- **Diseases:** B-aggressive lymphoma (MESH:D016393), BC (MESH:D001943), Cancer (MESH:D009369)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

9 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12288338/full.md

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Source: https://tomesphere.com/paper/PMC12288338