Urologic oncology · 2025
Exploring the tumor-promoting function and prognostic value of ESPL1 in prostate adenocarcinoma.
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Zhang Xuemei, Pan Peng, Wang Shuaijie, Chen Shaohua, Sun Yiping, Meng Xuan, Yang Yuzhong
Аннотация
BACKGROUND: Extra spindle pole bodies-like 1 (ESPL1), a gene encoding the Separase protein, has been implicated in cancer development across multiple tumor types. However, its precise role in prostate adenocarcinoma (PRAD) remains underexplored. This study investigates ESPL1's contribution to PRAD progression and evaluates its utility as a prognostic indicator and potential therapeutic target.
METHODS: We analyzed ESPL1 expression using datasets from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO). The prognostic significance of ESPL1 was evaluated through survival analysis. Tissue expression of ESPL1 was examined via immunohistochemistry (IHC). Additionally, Gene Set Enrichment Analysis (GSEA) was performed to identify related biological pathways. Functional roles were tested in PRAD cell lines through proliferation assays (colony formation, CCK-8, EdU), apoptosis assays (TUNEL, flow cytometry), and cell cycle analysis.
RESULTS: ESPL1 expression was markedly elevated in PRAD tissues opposed to normal prostate samples and correlated with advanced disease features, such as higher T and N stages and residual tumor presence. Survival analysis linked high ESPL1 levels to reduced overall survival (OS) and progression-free interval (PFI). GSEA identified enrichment in pathways tied to cell division and DNA repair. Suppressing ESPL1 in vitro diminished cell growth and triggered apoptosis in PRAD cells.
CONCLUSIONS: Our findings suggest that ESPL1 contributes to PRAD progression by regulating proliferation and apoptosis, potentially serving as both a prognostic biomarker and a candidate target for therapeutic development.
METHODS: We analyzed ESPL1 expression using datasets from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO). The prognostic significance of ESPL1 was evaluated through survival analysis. Tissue expression of ESPL1 was examined via immunohistochemistry (IHC). Additionally, Gene Set Enrichment Analysis (GSEA) was performed to identify related biological pathways. Functional roles were tested in PRAD cell lines through proliferation assays (colony formation, CCK-8, EdU), apoptosis assays (TUNEL, flow cytometry), and cell cycle analysis.
RESULTS: ESPL1 expression was markedly elevated in PRAD tissues opposed to normal prostate samples and correlated with advanced disease features, such as higher T and N stages and residual tumor presence. Survival analysis linked high ESPL1 levels to reduced overall survival (OS) and progression-free interval (PFI). GSEA identified enrichment in pathways tied to cell division and DNA repair. Suppressing ESPL1 in vitro diminished cell growth and triggered apoptosis in PRAD cells.
CONCLUSIONS: Our findings suggest that ESPL1 contributes to PRAD progression by regulating proliferation and apoptosis, potentially serving as both a prognostic biomarker and a candidate target for therapeutic development.