{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,24]],"date-time":"2026-06-24T16:59:46Z","timestamp":1782320386285,"version":"3.54.5"},"reference-count":39,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2025,4,26]],"date-time":"2025-04-26T00:00:00Z","timestamp":1745625600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Biochem &amp;amp; Molecular Tox"],"published-print":{"date-parts":[[2025,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Acute myeloid leukemia (AML) is a malignant tumor of blood cells, which seriously interferes with the generation of normal cells. Although miR\u2010186\u20105p is diminished in AML, its exact mechanism is not well understood. miR\u2010186\u20105p and PD\u2010L1 levels in AML cells (HL\u201060, KG\u20101, TF\u20101a, MOLT\u20103) and subcutaneous tumor tissue were discovered through qRT\u2010PCR and Western blot. miR\u2010186\u20105 p and PD\u2010L1 combining sites were foreseen by the database and verified by dual luciferase and immunoprecipitation experiments. AML cells with miR\u2010186\u20105p overexpression or knockdown and PD\u2010L1 overexpression were cocultured with CD4<jats:sup>+<\/jats:sup> and CD8<jats:sup>+<\/jats:sup> T cells. The proliferation, migration, invasion and apoptosis of AML cells, CD8<jats:sup>+<\/jats:sup> and CD4<jats:sup>+<\/jats:sup> T cell growth and apoptosis, and activated markers (Perforin and Granzyme B) and secreted cytokines (IFN\u2010\u03b3, IL\u20104 and TNF\u2010\u03b1) levels were detected by CCK8, Transwell, flow cytometry, CFSE, Western blot and ELISA, respectively. Subcutaneous xenograft magnitude and mass in nude mice were measured. Ki67 level was identified through immunohistochemistry. CD4<jats:sup>+<\/jats:sup> and CD8<jats:sup>+<\/jats:sup> T cell level and infiltration were detected by immunofluorescence and flow cytometry. miR\u2010186\u20105p was downregulated, and PD\u2010L1 was boosted in AML cells and subcutaneous tumor tissues (<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05), while miR\u2010186\u20105p targeted down\u2010regulate PD\u2010L1. miR\u2010186\u20105p upregulation hindered AML cell multiplication, migration, invasion and facilitate cell death, and enhanced the proliferation activity, activation markers (Perforin and Granzyme B) and secreted cytokines (IFN\u2010\u03b3, IL\u20104, TNF\u2010\u03b1) of CD8<jats:sup>+<\/jats:sup> and CD4<jats:sup>+<\/jats:sup> T cells, inhibited apoptosis, and inhibited immune escape (<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05). Knockdown of miR\u2010186\u20105p can promote AML progression, but PD\u2010L1 upregulation weakens the antitumor impact of miR\u2010186\u20105p overexpression (<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05). Transplanted tumor mice experiments also found that miR\u2010186\u20105p hindered PD\u2010L1 and tumor growth (<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05). In conclusion, miR\u2010186\u20105p can target inhibit PD\u2010L1, suppress AML cells multiplication, movement, invasion and immune escape, and then reduce AML, aiming to provide support and basis for the pathological mechanism and prevention and treatment strategy of AML.<\/jats:p>","DOI":"10.1002\/jbt.70278","type":"journal-article","created":{"date-parts":[[2025,4,26]],"date-time":"2025-04-26T04:46:54Z","timestamp":1745642814000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["miR\u2010186\u20105p Down\u2010Regulates PD\u2010L1 Level in Acute Myeloid Leukemia Cells and Inhibits Tumorigenesis and Immune Escape"],"prefix":"10.1002","volume":"39","author":[{"given":"Cheng","family":"Lian","sequence":"first","affiliation":[{"name":"Department of Hematology Henan provincial People's Hospital Zhengzhou Henan 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