# Recognition of HSPB8 as a potential therapeutic target for prostate cancer

**Authors:** Xun Fu, Yutao Wang, Hongjun Li

PMC · DOI: 10.3389/fgene.2025.1680674 · 2025-10-21

## TL;DR

This study identifies HSPB8 as a potential therapeutic target and tumor suppressor in prostate cancer, based on its expression patterns and biological functions.

## Contribution

The novel contribution is the identification of HSPB8 as a tumor suppressor and potential therapeutic target in prostate cancer.

## Key findings

- HSPB8 is underexpressed in prostate cancer tissues compared to normal tissues.
- Low HSPB8 expression correlates with poor survival outcomes in prostate cancer patients.
- HSPB8 silencing promotes cancer cell proliferation and migration via PI3K−AKT signaling inactivation.

## Abstract

Prostate cancer poses a serious burden on men’s quality of life. Identifying novel biomarkers for therapeutic development and prognostic prediction has long been a focal point in prostate cancer research. HSP family is a group of molecular chaperones that exhibit close relationship with many cancer types. In this study we screened out HSPB8 as a potential biomarker using WGCNA. Then we analyzed its expression patterns, investigated its biological functions, and assessed its prognostic values with a combination of bioinformatic analyses and experimental validation. Our data demonstrated that HSPB8 exhibited lower expression levels in prostate cancer tissues than in normal prostatic tissues. As a tumor suppressor gene, lack of HSPB8 was associated with unfavorable survival outcomes among patients with prostate cancer. In terms of biological function, HSPB8 were predominantly enriched in muscle-related biological processes, such as muscle contraction and muscle cell differentiation. On the molecular and cellular levels, HSPB8 silencing induced cellular proliferation and enhanced invasive and migratory capacities of prostate cancer cell lines. Its tumor-suppressive function was likely mediated through inactivation of PI3K−AKT signaling. Overall, this study offers a new understanding into the pathogenesis of prostate cancer, proposing that targeting HSPB8 might be a promising area in prostate cancer treatment.

## Linked entities

- **Genes:** HSPB8 (heat shock protein family B (small) member 8) [NCBI Gene 26353], PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) [NCBI Gene 5290], AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207]
- **Diseases:** prostate cancer (MONDO:0005159)

## Full-text entities

- **Genes:** HSPB8 (heat shock protein family B (small) member 8) [NCBI Gene 26353] {aka CMT2L, DHMN2, E2IG1, H11, HMN2, HMN2A}, PIK3CB (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta) [NCBI Gene 5291] {aka P110BETA, PI3K, PI3KBETA, PIK3C1}, AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}
- **Diseases:** Prostate cancer (MESH:D011471), cancer (MESH:D009369)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

9 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12582549/full.md

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Source: https://tomesphere.com/paper/PMC12582549