{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,7]],"date-time":"2026-08-07T16:10:30Z","timestamp":1786119030362,"version":"build-2736575974"},"reference-count":56,"publisher":"Public Library of Science (PLoS)","issue":"8","license":[{"start":{"date-parts":[[2026,8,6]],"date-time":"2026-08-06T00:00:00Z","timestamp":1785974400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100003819","name":"Natural Science Foundation of Hubei Province","doi-asserted-by":"publisher","award":["2025AFB931"],"award-info":[{"award-number":["2025AFB931"]}],"id":[{"id":"10.13039\/501100003819","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.plosone.org"],"crossmark-restriction":false},"short-container-title":["PLoS One"],"abstract":"<jats:sec id=\"sec001\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>As the most common malignant renal tumor in children, the progression of Wilms\u2019 tumor is frequently driven by abnormal alternative splicing (AS), cell death imbalance, and an immunosuppressive microenvironment. However, the precise regulatory chain connecting these three critical elements remains largely unexplored. This study aimed to systematically construct and characterize an \u201cAS-cell death-immunity\u201d regulatory network in Wilms\u2019 tumor.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"sec002\">\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We performed a comprehensive\n                      <jats:italic>in silico<\/jats:italic>\n                      analysis using matched paired Wilms\u2019 tumor and adjacent normal RNA-seq data from the GSE138869 cohort. The SUVA algorithm was employed to identify cell death-related regulated alternative splicing events (RASEs). A tripartite regulatory network was constructed via correlation analysis to link these RASEs with upstream differentially expressed splicing factors (DESFs). Immune cell infiltration was quantified using CIBERSORT. Finally, the\n                      <jats:italic>HNRNPD<\/jats:italic>\n                      knockout and FLASH-seq multi-omics dataset (GSE212767) was utilized to computationally validate the predicted regulatory axis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"sec003\">\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Our analysis identified 118 cell death-related host genes undergoing significant alternative splicing in Wilms\u2019 tumor. Network integration highlighted a critical regulatory axis where the overexpressed splicing factor\n                      <jats:italic>HNRNPD<\/jats:italic>\n                      is strongly correlated with an aberrant AS event (clualt5p51764) in the apoptosis-related kinase\n                      <jats:italic>MAP4K4<\/jats:italic>\n                      . Further immune deconvolution demonstrated that both\n                      <jats:italic>HNRNPD<\/jats:italic>\n                      upregulation and the\n                      <jats:italic>MAP4K4<\/jats:italic>\n                      splicing shift were significantly correlated with increased monocyte infiltration in the tumor microenvironment. Moreover, cross-validation utilizing the GSE212767 dataset confirmed that\n                      <jats:italic>HNRNPD<\/jats:italic>\n                      perturbation directly alters\n                      <jats:italic>MAP4K4<\/jats:italic>\n                      splicing.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"sec004\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Our computational framework proposes that the\n                      <jats:italic>HNRNPD<\/jats:italic>\n                      -\n                      <jats:italic>MAP4K4<\/jats:italic>\n                      splicing axis links apoptotic dysregulation to immune microenvironment remodeling in Wilms\u2019 tumor. These correlative\n                      <jats:italic>in silico<\/jats:italic>\n                      findings provide a robust, hypothesis-generating basis for discovering novel prognostic biomarkers and developing targeted therapeutic strategies directed at the splicing machinery.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1371\/journal.pone.0354712","type":"journal-article","created":{"date-parts":[[2026,8,6]],"date-time":"2026-08-06T17:25:17Z","timestamp":1786037117000},"page":"e0354712","update-policy":"https:\/\/doi.org\/10.1371\/journal.pone.corrections_policy","source":"Crossref","is-referenced-by-count":0,"title":["Splicing factor HNRNPD and alternative splicing of MAP4K4 are associated with cell apoptosis and immune microenvironment features in Wilms\u2019 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