The oncogenic role of mir-21 in cervical cancer: linking epithelial–mesenchymal transition to stromal remodeling

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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 in vitro cell-line experiments, tissue-based clinical studies, and mixed models; findings were interpreted according to their level of evidence. 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 in vitro 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.

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