Cancer biology & therapy · 2026
Retinol dehydrogenase 11 promotes prostate cancer progression through upregulation of tropomyosin receptor kinase A.
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Wang Shenghan, Zhang Shuyu, Xin Zekun, Lei Zhentao, Xiong Jie, Shi Yuqiang, Yang Lin, Gao Qiang, Le Kai, Zhang Bao
Аннотация
OBJECTIVE: To clarify the clinical significance and biological function of retinol dehydrogenase-11 (RDH11) in prostate cancer (PCa) and to elucidate the downstream signaling mechanism through which it drives tumor progression.
METHODS: Public and in-house transcriptomic data were mined to compare RDH11 levels between PCa and matched normal tissues. RDH11 was stably silenced (shRDH11) or over-expressed (oeRDH11) in PC-3, DU145, and LNCaP cells; cell proliferation, migration, and invasion were quantified with CCK-8 and Transwell assays. RNA-seq and gene set enrichment analysis (GSEA) were performed to screen downstream targets and pathways. Rescue experiments in vitro and in vivo were used to confirm the mechanism.
RESULTS: RDH11 levels were markedly elevated in human PCa tissues and cell lines. Silencing RDH11 hindered PCa cell proliferation, migration, and invasion, whereas its overexpression had the opposite effects. Mechanistically, we identified the tropomyosin receptor kinase (TRKA) and STAT3 signaling pathway as the downstream gene and pathway of RDH11. Rescue assays using PC3, DU145, and LNCaP cells demonstrated that RDH11 facilitated PCa progression by upregulation of TRKA and the activation of STAT3 signaling. In vivo studies further confirmed that RDH11 overexpression enhanced prostate tumor growth, whereas TRKA knockdown counteracted the oncogenic effects of RDH11.
CONCLUSION: RDH11 promotes the development of PCa through the upregulation of TRKA and activation of the STAT3 signaling pathway.
METHODS: Public and in-house transcriptomic data were mined to compare RDH11 levels between PCa and matched normal tissues. RDH11 was stably silenced (shRDH11) or over-expressed (oeRDH11) in PC-3, DU145, and LNCaP cells; cell proliferation, migration, and invasion were quantified with CCK-8 and Transwell assays. RNA-seq and gene set enrichment analysis (GSEA) were performed to screen downstream targets and pathways. Rescue experiments in vitro and in vivo were used to confirm the mechanism.
RESULTS: RDH11 levels were markedly elevated in human PCa tissues and cell lines. Silencing RDH11 hindered PCa cell proliferation, migration, and invasion, whereas its overexpression had the opposite effects. Mechanistically, we identified the tropomyosin receptor kinase (TRKA) and STAT3 signaling pathway as the downstream gene and pathway of RDH11. Rescue assays using PC3, DU145, and LNCaP cells demonstrated that RDH11 facilitated PCa progression by upregulation of TRKA and the activation of STAT3 signaling. In vivo studies further confirmed that RDH11 overexpression enhanced prostate tumor growth, whereas TRKA knockdown counteracted the oncogenic effects of RDH11.
CONCLUSION: RDH11 promotes the development of PCa through the upregulation of TRKA and activation of the STAT3 signaling pathway.