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Alternative polyadenylation (APA) is an important post\u2010transcriptional mechanism, and its dysregulation is closely linked to the pathogenesis of hematological malignancies. This study aimed to clarify the regulatory role of the NUDT21\u2010APA\u2010SRSF2 axis in the progression of myelodysplastic syndrome (MDS). To this end, we established MDS cell models overexpressing or knocking down NUDT21 and SRSF2. The regulatory mechanism and functional impacts of this axis were systematically evaluated using RT\u2010qPCR, Western blot, CCK\u20108 assay and flow cytometry; APA site analysis mediated by specific primers and transcriptome sequencing. The results showed that the expression of NUDT21 was negatively correlated with that of SRSF2 (\n                    <jats:italic>p\u00a0&lt;<\/jats:italic>\n                    \u00a00.05). Overexpression of NUDT21 promoted the utilisation of distal polyadenylation sites on\n                    <jats:italic>SRSF2<\/jats:italic>\n                    , increasing the expression of its long 3\u2032UTR variants; conversely, NUDT21 knockdown produced the opposite effect (\n                    <jats:italic>p\u00a0&lt;<\/jats:italic>\n                    \u00a00.05). Functionally, NUDT21 enhanced MDS cell proliferation and inhibited apoptosis, though this effect was reversed by co\u2010overexpression of SRSF2. Furthermore, SRSF2 could antagonize the regulatory effect of NUDT21 on the cell cycle. In summary, our in vitro data demonstrate that NUDT21 remodels SRSF2 isoform balance via alternative polyadenylation (APA) and regulates biological functions of MDS\u2010derived cells. The NUDT21\u2010APA\u2010SRSF2 axis represents a key regulatory cascade with potential therapeutic implications.\n                  <\/jats:p>","DOI":"10.1002\/hon.70255","type":"journal-article","created":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T17:35:39Z","timestamp":1790962539000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["NUDT21 Promotes Myelodysplastic Syndrome Progression by Regulating SRSF2 Expression via Alternative Polyadenylation"],"prefix":"10.1002","volume":"44","author":[{"ORCID":"https:\/\/orcid.org\/0009-0005-7731-4176","authenticated-orcid":false,"given":"Dongmei","family":"Guan","sequence":"first","affiliation":[{"name":"Shanxi Medical University  Taiyuan Shanxi Province China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wenjie","family":"Xu","sequence":"additional","affiliation":[{"name":"Shanxi Medical University  Taiyuan Shanxi Province China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shuo","family":"Li","sequence":"additional","affiliation":[{"name":"Shanxi Medical University  Taiyuan Shanxi Province China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peichun","family":"Li","sequence":"additional","affiliation":[{"name":"Shanxi Medical University  Taiyuan Shanxi Province China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiakai","family":"Bian","sequence":"additional","affiliation":[{"name":"Shanxi Medical University  Taiyuan Shanxi Province China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2902-591X","authenticated-orcid":false,"given":"HongWei","family":"Wang","sequence":"additional","affiliation":[{"name":"Shanxi Medical University  Taiyuan Shanxi Province China"},{"name":"Shanxi Key Laboratory of Molecular Diagnosis and Treatment of Hematological Diseases Department of Hematology The Second Hospital of Shanxi Medical University  Taiyuan Shanxi Province China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fanggang","family":"Ren","sequence":"additional","affiliation":[{"name":"Shanxi Medical University  Taiyuan Shanxi Province China"},{"name":"Shanxi Key Laboratory of Molecular Diagnosis and Treatment of Hematological Diseases Department of Hematology The Second Hospital of Shanxi Medical University  Taiyuan Shanxi Province China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,10,2]]},"reference":[{"key":"e_1_2_9_2_1","doi-asserted-by":"publisher","DOI":"10.1038\/s41375\u2010022\u201001613\u20101"},{"key":"e_1_2_9_3_1","doi-asserted-by":"publisher","DOI":"10.1182\/blood.2022015850"},{"key":"e_1_2_9_4_1","doi-asserted-by":"publisher","DOI":"10.3390\/life14050637"},{"key":"e_1_2_9_5_1","doi-asserted-by":"publisher","DOI":"10.1038\/s41571\u2010026\u201001141\u20102"},{"key":"e_1_2_9_6_1","doi-asserted-by":"publisher","DOI":"10.1038\/ncomms15099"},{"key":"e_1_2_9_7_1","doi-asserted-by":"crossref","first-page":"417","DOI":"10.1007\/978-1-4419-5698-9_33","volume-title":"Molecular Pathology of Hematolymphoid Diseases","author":"Taylor J. 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