{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,21]],"date-time":"2026-08-21T13:44:04Z","timestamp":1787319844918,"version":"build-2736575974"},"reference-count":45,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,5,25]],"date-time":"2026-05-25T00:00:00Z","timestamp":1779667200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Oncol."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>Acute myeloid leukemia (AML) remains a heterogeneous hematologic malignancy with frequent therapeutic resistance and relapse. Although miR-2110 is upregulated in AML, its functional role and downstream mechanism remain unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Publicly available miRNA-sequencing data were analyzed to identify dysregulated miRNAs in AML. miR-2110 expression was validated in AML cell lines. Functional assays, including CCK-8, EdU incorporation, apoptosis analysis, western blotting, dual-luciferase reporter assays, rescue experiments, Ara-C sensitivity assays, and xenograft experiments, were performed to evaluate the role of miR-2110 and its downstream target.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      miR-2110 was upregulated in AML samples and cell lines but exerted tumor-suppressive effects. miR-2110 overexpression inhibited AML cell proliferation, reduced cell-cycle\u2013related protein expression, and promoted apoptosis-related changes. ELK1 was identified and validated as a direct target of miR-2110 through multiple predicted binding sites within its 3\u2032UTR. Restoration of ELK1 partially reversed miR-2110-associated molecular changes, supporting ELK1 as an important downstream mediator. miR-2110 also enhanced Ara-C responsiveness in parental and resistant AML cells, while Ara-C-resistant cells showed reduced miR-2110 and increased ELK1 expression.\n                      <jats:italic>In vivo<\/jats:italic>\n                      , miR-2110 overexpression suppressed xenograft tumor growth without obvious body weight loss.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>miR-2110 functions as an upregulated but tumor-suppressive miRNA in AML. The miR-2110\u2013ELK1 axis contributes to regulation of AML cell growth, apoptosis-related signaling, and Ara-C responsiveness, providing a potential molecular basis for further investigation of miRNA-mediated therapeutic modulation in AML.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fonc.2026.1833649","type":"journal-article","created":{"date-parts":[[2026,5,25]],"date-time":"2026-05-25T04:42:45Z","timestamp":1779684165000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["miR-2110 orchestrates ERK\u2013ELK1 transcriptional repression to induce cell-cycle arrest and enhance cytarabine sensitivity in acute myeloid leukemia"],"prefix":"10.3389","volume":"16","author":[{"given":"Ya","family":"Li","sequence":"first","affiliation":[{"name":"Department of Hematology, Affiliated Hospital of Guizhou Medical University","place":["Guiyang, Guizhou, 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