# High SRD5A3 expression is correlated with promotion of proliferation and inhibition of apoptosis in B-cell non-Hodgkin lymphoma and suggests a poor prognosis

**Authors:** Shanshan Wei, Jie Sun, Jiahao Wen, Jianing Yu, Yixuan Xuan, Jingyu Huang, Jie Yang, Jianfeng Zhang

PMC · DOI: 10.1371/journal.pone.0323965 · PLOS One · 2025-05-21

## TL;DR

High SRD5A3 expression in B-cell non-Hodgkin lymphoma is linked to faster cancer growth, less cell death, and worse patient survival, suggesting it could be a new target for treatment.

## Contribution

This study identifies SRD5A3 as a novel biomarker and potential therapeutic target in B-cell non-Hodgkin lymphoma via the PI3K-AKT pathway.

## Key findings

- High SRD5A3 expression correlates with poor prognosis in B-NHL patients.
- SRD5A3 promotes B-NHL cell proliferation and inhibits apoptosis.
- SRD5A3 activates the PI3K-AKT signaling pathway to drive oncogenic effects.

## Abstract

Steroid 5α-reductase 3 (SRD5A3) is an important molecule involved in glycosylation and steroid hormone formation and is highly expressed in most tumors. However, The role of SRD5A3 in B-cell non-Hodgkin lymphoma (B-NHL) and its mechanism are unknown.

We used a multi-omics database to explore the expression and prognostic significance of SRD5A3 in various tumors, including B-NHL. We established SRD5A3 high- and low-expression B-NHL cell lines to test the effects of SRD5A3 on cell proliferation and apoptosis in vitro, and to analyze the signaling pathways associated with the effects of SRD5A3 on B-NHL.

We found that SRD5A3 was highly expressed in most tumors, including B-NHL, and was more highly expressed in patients age ≥60 years, high levels of LDH, stage III-IV, non-GCB subtype, and extra-nodal invasion. Survival analysis showed that high SRD5A3 expression predicted poorer overall survival (OS). Further experiments showed that SRD5A3 high expression promoted B-NHL growth and attenuates apoptosis, conversely, SRD5A3 low expression inhibited B-NHL growth and promoted apoptosis. Western blot assay showed SRD5A3 promotes B-NHL cells growth by regulating the PI3K-AKT signaling pathway.

Our findings suggest that SRD5A3 exerts its oncogenic effects by regulating the PI3K-AKT pathway, may serve as a potential biomarker and therapeutic target for B-NHL, providing information for clinical decision-making.

## Linked entities

- **Genes:** SRD5A3 (steroid 5 alpha-reductase 3) [NCBI Gene 79644], PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) [NCBI Gene 5290], AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207]
- **Diseases:** B-cell non-Hodgkin lymphoma (MONDO:0015759)

## Full-text entities

- **Genes:** 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}, SRD5A3 (steroid 5 alpha-reductase 3) [NCBI Gene 79644] {aka CDG1P, CDG1Q, KRIZI, S5AR, S5AR 3, SRD5A2L}
- **Diseases:** tumors (MESH:D009369), B-NHL (MESH:D016393)
- **Chemicals:** steroid hormone (MESH:D013256)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

13 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12094769/full.md

## References

40 references — full list in the complete paper: https://tomesphere.com/paper/PMC12094769/full.md

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Source: https://tomesphere.com/paper/PMC12094769