{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,3]],"date-time":"2026-08-03T01:46:24Z","timestamp":1785721584042,"version":"3.56.0"},"reference-count":31,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2026,4,16]],"date-time":"2026-04-16T00:00:00Z","timestamp":1776297600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,4,16]],"date-time":"2026-04-16T00:00:00Z","timestamp":1776297600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Oral Pathology Medicine"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>Emerging evidence underscores the potential of ferroptosis as a promising therapeutic target in cancer. However, the role of microRNAs (miRNAs) in modulating ferroptosis sensitivity remains largely unexplored, particularly in the context of oral squamous cell carcinoma (OSCC) chemoresistance. This study was designed to investigate the role of miR\u2010214\u20103p in regulating ferroptosis by targeting glutathione peroxidase 4 (GPX4) and its influence on cisplatin (DDP) resistance in OSCC.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Patients diagnosed with OSCC and receiving DDP\u2010based chemotherapy between February 2022 and February 2024 at our institution were included in this study. Expression levels of miR\u2010214\u20103p and GPX4 were quantitatively assessed in DDP\u2010sensitive versus DDP\u2010resistant OSCC tissues and cell lines using qRT\u2010PCR and Western blot. Cell viability, IC50 values, and apoptosis were evaluated using the CCK\u20108 assay and flow cytometry. Intracellular reactive oxygen species (ROS) and Fe\n                      <jats:sup>2+<\/jats:sup>\n                      levels were measured to determine the status of ferroptosis. Bioinformatics prediction and dual\u2010luciferase reporter assays confirmed the interaction between miR\u2010214\u20103p and GPX4. In\u00a0vivo xenograft models were utilized to investigate the impact of miR\u2010214\u20103p on OSCC tumor growth.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      As an initial assessment of clinical relevance, miR\u2010214\u20103p was significantly downregulated in DDP\u2010resistant OSCC tissues and cells, whereas GPX4 expression was markedly upregulated. Overexpression of miR\u2010214\u20103p substantially decreased cell viability, reduced the IC\n                      <jats:sub>50<\/jats:sub>\n                      values of DDP, and promoted apoptosis in resistant cells. In comparison to parental cells, resistant cells demonstrated lower levels of ROS and Fe\n                      <jats:sup>2+<\/jats:sup>\n                      . Overexpression of miR\u2010214\u20103p or treatment with a ferroptosis inducer (Erastin) increased ROS and Fe\n                      <jats:sup>2+<\/jats:sup>\n                      levels, an effect that was effectively reversed by a ferroptosis inhibitor (Ferrostatin\u20101). Bioinformatics analysis combined with luciferase reporter assays confirmed the direct binding of miR\u2010214\u20103p to the 3\u2032 untranslated region (UTR) of GPX4. The overexpression of miR\u2010214\u20103p resulted in the downregulation of GPX4, whereas overexpression of GPX4 reversed the effects mediated by miR\u2010214\u20103p. Additionally, the overexpression of miR\u2010214\u20103p in xenograft models inhibited tumor growth, which was correlated with decreased GPX4 expression and increased sensitivity to DDP.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Our findings reveal a novel miR\u2010214\u20103p\/GPX4\/ferroptosis axis in OSCC DDP resistance. miR\u2010214\u20103p suppresses GPX4 to promote ferroptosis, thereby reversing DDP resistance. This study identifies miR\u2010214\u20103p as a potential therapeutic target for overcoming chemoresistance in OSCC by modulating ferroptosis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/jop.70138","type":"journal-article","created":{"date-parts":[[2026,4,17]],"date-time":"2026-04-17T04:31:49Z","timestamp":1776400309000},"page":"793-804","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Effect of\n                    <scp>miR<\/scp>\n                    \u2010214\u20103p on Cisplatin Resistance in Oral Squamous Cell Carcinoma by Regulating Ferroptosis Through Targeting\n                    <scp>GPX4<\/scp>"],"prefix":"10.1111","volume":"55","author":[{"given":"Rongxia","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Stomatology The Second Hospital of Shijiazhuang  Shijiazhuang Hebei People's Republic of 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