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However, the molecular mechanisms underlying RRD remain poorly understood. In this study, a radiation recall\u2013like dermatitis model (RRLD) was established in Sprague\u2013Dawley rats by localized skin irradiation followed by subcutaneous administration of non-toxic concentrations of chemotherapeutic agents, including 5-fluorouracil (5-Fu, 10 \u00b5g\/\u00b5L) or Epirubicin (EPI, 0.05 \u00b5g\/\u00b5L), into the irradiated area. Transcriptomic and miRNA sequencing of rat skin tissues from RRLD rats identified a panel of dysregulated miRNAs, among which miR-338-3p was the most prominently upregulated and was further corroborated by elevated miR-338-3p levels in serum samples from patients with RRD. Dual-luciferase reporter assays demonstrated that pleiotrophin (PTN) is a direct target of miR-338-3p. Functional studies showed that miR-338-3p overexpression in HaCaT and WS1 cells significantly enhanced apoptotic cell death and exacerbated radiation recall\u2013associated cellular injury, whereas miR-338-3p inhibition attenuated apoptosis and promoted cellular recovery. In vivo, pharmacological or genetic inhibition of miR-338-3p, as well as activation of PTN, significantly alleviated the severity of RRLD. Enrichment analyses indicated that miR-338-3p\u2013mediated suppression of PTN resulted in downregulation of the PI3K\/Akt\/Bcl2 signaling pathway, thereby compromising pro-survival signaling cascades. Consistently, rescue experiments using an Akt activator (SC79) partially restored p-Akt and Bcl2 expression and markedly reduced apoptotic responses, supporting the functional relevance of this pathway in RRLD. Collectively, these findings indicate that miR-338-3p acts as a critical epigenetic regulator of RRLD through modulation of the PTN\/PI3K\/Akt\/Bcl2 axis and suggest that this molecular circuit represents a promising therapeutic target for mitigating clinical radiation recall\u2013associated skin injury.<\/jats:p>","DOI":"10.1186\/s43556-026-00424-5","type":"journal-article","created":{"date-parts":[[2026,3,9]],"date-time":"2026-03-09T02:09:23Z","timestamp":1773022163000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["miR-338-3p promotes radiation recall like dermatitis by suppressing pleiotrophin via the PI3K\/Akt\/Bcl2 pathway"],"prefix":"10.1186","volume":"7","author":[{"given":"Yu","family":"Min","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jingjing","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yahui","family":"Feng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ping","family":"Yang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaopeng","family":"Xu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jun","family":"Dai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shuyu","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7042-718X","authenticated-orcid":false,"given":"Xingchen","family":"Peng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,3,9]]},"reference":[{"issue":"12","key":"424_CR1","doi-asserted-by":"publisher","first-page":"1892","DOI":"10.1038\/s41565-024-01784-1","volume":"19","author":"Y Liao","year":"2024","unstructured":"Liao Y, Wang D, Gu C, Wang X, Zhu S, Zheng Z, et al. 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