{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T12:55:17Z","timestamp":1792760117663,"version":"4.5.0"},"reference-count":62,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,8,3]],"date-time":"2026-08-03T00:00:00Z","timestamp":1785715200000},"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>Background<\/jats:title>\n                    <jats:p>Cervical cancer remains a leading cause of cancer mortality worldwide, driven primarily by persistent infection with oncogenic human papillomavirus (HPV). Epithelial\u2013mesenchymal transition (EMT) is a critical process in tumor invasion and metastasis, and miR-21 has been identified as a frequently upregulated oncomiR whose locus at 17q23.2 overlaps a common HPV16 integration site and which simultaneously targets multiple tumor suppressors, positioning it as a candidate convergent oncomiR with proposed regulatory roles in both processes.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>This review synthesizes current knowledge on the oncogenic role of miR-21 in cervical cancer, with particular emphasis on its dual function in EMT and stromal remodeling.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We conducted a narrative review of published studies identified through PubMed, Scopus, Web of Science and Embase. Included studies were heterogeneous in design, comprising\n                      <jats:italic>in vitro<\/jats:italic>\n                      cell-line experiments, tissue-based clinical studies, and mixed models; findings were interpreted according to their level of evidence.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key findings<\/jats:title>\n                    <jats:p>miR-21 is frequently upregulated in HPV-positive cervical cancer cell lines and tissue specimens, where it has been shown \u2014 predominantly in preclinical models \u2014 to suppress tumor suppressors, downregulate epithelial markers, and upregulate mesenchymal markers. It is also enriched in tumor-associated fibroblasts in experimental models, where it has been associated with fibroblast activation and extracellular matrix remodeling. Preclinical inhibition of miR-21 reverses EMT markers and improves chemosensitivity in cell-line models.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      This review integrates evidence across miR-21, EMT, and stromal remodeling in cervical cancer, proposing a conceptual framework in which miR-21 functions as a convergent regulator linking tumor cell EMT to fibroblast-driven stromal remodeling\u2014 a synthesis not previously proposed in the literature. The current evidence, mainly based on\n                      <jats:italic>in vitro<\/jats:italic>\n                      and cell-line studies conducted in Asian populations, supports the biological plausibility of this role; however, it has not yet established a causal relationship in human cervical cancer. Patient-level validation in diverse, well-characterized cohorts is needed before miR-21 can be considered a clinically actionable biomarker or therapeutic target.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fonc.2026.1814515","type":"journal-article","created":{"date-parts":[[2026,8,11]],"date-time":"2026-08-11T15:15:55Z","timestamp":1786461355000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["The oncogenic role of mir-21 in cervical cancer: linking epithelial\u2013mesenchymal transition to stromal remodeling"],"prefix":"10.3389","volume":"16","author":[{"given":"Ingrid","family":"Galvis","sequence":"first","affiliation":[{"name":"Department of Radiology, Jacobi Medical Center","place":["New York City, NY, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aiman","family":"Hafeez","sequence":"additional","affiliation":[{"name":"Department of 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