DUSP13 promotes prostate cancer progression by regulating the ERK1/2 pathway.

Authors

Qing Lu, Xiaobao Chen, Zhenlin Chen, Jing Lin, Yiming Su

Published in

Translational andrology and urology. Volume 15. Issue 9. Pages 327. Sep 30, 2026. Epub Aug 31, 2026.

Abstract

Prostate cancer (PCa) remains a leading cause of cancer-related morbidity and mortality in men, and patients who progress to castration-resistant prostate cancer (CRPC) derive only limited benefit from currently available treatments; novel therapeutic targets are therefore urgently needed. Dual specificity phosphatase 13 (DUSP13) belongs to the DUSP family, whose members dephosphorylate mitogen-activated protein kinases (MAPKs) and display either tumor-suppressive or tumor-promoting activity in a context-dependent manner. Emerging evidence implicates DUSP13 in several malignancies, but its expression and function in PCa, and whether it acts through the ERK1/2 pathway, remain unknown. This study aimed to elucidate the function of DUSP13 in PCa.
DUSP13 expression in the normal prostate epithelial-derived cell line RWPE-1 and in the PCa cell lines PC-3, DU145 and LNCaP was examined by Western blot and quantitative reverse transcription polymerase chain reaction (qRT-PCR). DUSP13 was silenced in PC-3 and DU145 cells using lentiviral short hairpin RNAs (shRNAs); a second, independent shRNA targeting a distinct site was used to exclude off-target effects. Cell proliferation, migration, invasion and apoptosis were assessed by cell counting kit-8 (CCK-8), wound-healing (scratch), transwell and flow cytometry assays, respectively. Tumor growth was evaluated in a PC-3 subcutaneous xenograft model in BALB/c nude mice. Proteins of the ERK1/2 pathway were detected by Western blot, and the MAPK/ERK kinase (MEK) inhibitor PD98059 was used in rescue experiments.
DUSP13 protein and mRNA levels were higher in PCa cells than in RWPE-1 cells. DUSP13 knockdown suppressed proliferation, migration and invasion, promoted apoptosis, and attenuated xenograft tumor growth in vivo. Mechanistically, DUSP13 knockdown increased p-ERK1/2 levels, whereas PD98059 alone did not significantly alter proliferation, invasion or apoptosis and partially reversed the anti-tumor phenotypes induced by DUSP13 knockdown. All key findings were reproduced with a second independent shRNA.
DUSP13 promotes PCa progression by inhibiting ERK1/2 phosphorylation, suggesting that targeting DUSP13 may be a potential therapeutic strategy for PCa, including castration-resistant disease.

PMID:
42866857
Bibliographic data and abstract were imported from PubMed on 14 Oct 2026.

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