PubMed · 41517957
Proteomic analysis of cisplatin-induced spermatogenesis defects in mice.
Abstract
BACKGROUND: Cisplatin is a crucial chemotherapeutic agent used for treating various cancers; however, its excessive use can cause irreversible damage to the reproductive system, and the protein expression profile of cisplatin-induced testicular injury remains unclear. METHODS: Male C57BL/6 mice were treated with cisplatin at various doses, and testes were collected for histological, immunofluorescence, and proteomic analyses. Germ cell loss and apoptosis were assessed using H&E staining, TUNEL assays, and immunofluorescence for LIN28A, SYCP3, MVH, and CDK1. Label-free quantitative proteomics identified differentially expressed proteins, which were analyzed for functional enrichment and protein-protein interactions. RESULTS: We observed that cisplatin treatment led to smaller testes, reduced sperm count, and a significant decrease in the number of spermatocytes and spermatids in mice. Label-free quantitative proteomic analysis revealed that cisplatin significantly reduced the expression of cyclin-dependent kinase 1 (CDK1), a key spermatogenesis regulator, in the testes. Reduction in CDK1 expression is correlated with spermatogenic arrest, particularly in spermatocytes. CONCLUSION: These findings highlight the critical role of CDK1 in cisplatin-induced spermatogenic dysfunction and provide new insights into fertility preservation strategies for patients with cancer undergoing chemotherapy.
Explore related subjects
Keep this discovery
Pengyu Li, Ziran Chen, Zexuan Zhang, Hongbin Li, Yingnan Zhang. 2026-01-09. Proteomic analysis of cisplatin-induced spermatogenesis defects in mice.. https://doi.org/10.1080/07853890.2026.2612816
Cite the original work for its findings. Save a collection to share your selection of sources.
Discover connections
Connections use source metadata and explicit phrase matches, not verified experimental comparisons.