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NEPC is a highly aggressive subtype with poor prognosis and limited treatment options. Tumor\u2010associated macrophages (TAMs) contribute to tumor progression through exosome\u2010mediated communication. In our previous study, we analyzed RNA\u2010\n                    <jats:styled-content>s<\/jats:styled-content>\n                    eq data to identify key genes involved in PCa progression, and the RERG gene emerged as a significant candidate that suppresses neuroendocrine differentiation (NED). In this study, we demonstrate that RERG expression is significantly reduced in CRPC cells and NEPC tissues, and its downregulation activates the Ras\/ERK signaling pathway, which plays a crucial role in promoting NED. Additionally, miR\u2010142\u20105p, transferred from TAMs via exosomes, downregulates RERG expression and activates the Ras\/ERK pathway, thereby promoting PCa progression and NED. In\u00a0vitro, miR\u2010142\u20105p enhanced PCa cell proliferation, migration, invasion, and NED, while RERG overexpression reversed these effects. In\u00a0vivo, RERG knockdown significantly promoted tumor growth and NED in a xenograft model. These findings highlight the role of TAM\u2010derived miR\u2010142\u20105p in regulating NED and suggest that targeting the RERG\/Ras\/ERK axis may provide a novel therapeutic approach for NEPC.\n                  <\/jats:p>","DOI":"10.1096\/fj.202600930r","type":"journal-article","created":{"date-parts":[[2026,7,15]],"date-time":"2026-07-15T15:28:32Z","timestamp":1784129312000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Tumor\u2010Associated Macrophage Exosomal\n                    <scp>miR<\/scp>\n                    \u2010142\u20105p Drives\u00a0Prostate Cancer Neuroendocrine Differentiation via\u00a0\n                    <scp>RERG<\/scp>\n                    \/Ras\/\n                    <scp>ERK<\/scp>\n                    Axis"],"prefix":"10.1096","volume":"40","author":[{"given":"Bo\u2010Han","family":"Lin","sequence":"first","affiliation":[{"name":"Department of Urology, Urology Research Institute, the 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