ReviewFrontiers in oncology2026
The oncogenic role of mir-21 in cervical cancer: linking epithelial-mesenchymal transition to stromal remodeling.
Review in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Cervical cancer remains a leading cause of cancer mortality worldwide, driven primarily by persistent infection with oncogenic human papillomavirus (HPV). Epithelial-mesenchymal 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. Objective: 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. Methods: We conducted a narrative review of published studies identified through PubMed, Scopus, Web of Science and Embase. Included studies were heterogeneous in design, comprising Key findings: miR-21 is frequently upregulated in HPV-positive cervical cancer cell lines and tissue specimens, where it has been shown - predominantly in preclinical models - 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. Conclusion: 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- a synthesis not previously proposed in the literature. The current evidence, mainly based on
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