ArticleCellular and molecular life sciences : CMLS2025
The transcriptional regulation of NUPR1 expression by MYC is implicated in the regulation of ferroptosis in human spermatogonial stem cells.
Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Non-obstructive azoospermia (NOA) is a leading cause of male infertility, characterized by impaired spermatogenesis. Recent studies suggest that ferroptosis, an iron-dependent form of cell death, may contribute to testicular dysfunction, however, its role in NOA remains underexplored. In this study, we investigated the roles of NUPR1 and MYC in regulating ferroptosis in human spermatogonial stem cells (SSCs) and evaluated their potential as therapeutic targets for NOA. Single-cell RNA sequencing of testicular tissues from NOA and obstructive azoospermia (OA) patients revealed distinct cellular populations, with UMAP clustering showing a significant reduction in germ cells in NOA samples. High-dimensional weighted gene co-expression network analysis (hdWGCNA) identified two key modules (red and green-yellow) that were associated with spermatogonia. Integrative analysis of scRNA-seq, microarray datasets, and ferroptosis-related genes identified NUPR1 as a key regulatory gene. Immunofluorescence analysis demonstrated NUPR1 co-localization with SSC markers PLZF and UCHL1, and its expression was significantly lower in the testes of NOA patients compared to fertile controls. NUPR1 knockdown in SSCs led to increased ROS levels, lipid peroxidation, and Fe
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