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Moreover, aberrant epigenetic silencing (e.g. promoter hypermethylation) and interference by competing endogenous RNAs – including long non‐coding RNAs like MCF2L‑AS1 and DANCR as well as circular RNAs such as circ_0001588 – further diminish miR‐874’s expression and tumor‐suppressive activity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond oncogenesis, miR‐874 also plays pivotal roles in non‐malignant contexts. Studies have demonstrated that miR‐874 modulates inflammatory and cell death pathways in cardiovascular settings – for example, its down‐regulation contributes to sepsis‐induced myocardial dysfunction and exacerbates ischemia–reperfusion injury via altered STAT3/JAK2 signaling. In bone biology, miR‐874 promotes osteogenic differentiation of mesenchymal stem cells through repression of leptin, while in placental trophoblasts its targeting of USP8 facilitates proper cell proliferation and invasion—a mechanism potentially relevant to pre‐eclampsia. Collectively, these findings underscore the multifunctional role of miR‐874 as a critical regulator of both malignant and non‐malignant processes, offering promising opportunities for therapeutic intervention and improved prognostication."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "29", "end_ref": "32"}]}, {"type": "t", "text": ""}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "N Nohata, T Hanazawa, T Kinoshita, et al. 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