{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMicroRNA‐30c and its variants (including miR‐30c‐2*, miR‐30c‐1‐3p, and miR‐30c‐5p) have emerged as important regulators of diverse cellular processes, particularly in cancer. In several studies, miR‐30c was shown to act as a tumor suppressor by inhibiting epithelial‐to‐mesenchymal transition, cell proliferation, migration, invasion, and chemoresistance. For example, in breast cancer cells, miR‐30c suppresses chemoresistance by directly targeting the actin‐binding protein twinfilin 1 and modulating interleukin‐11 signaling, while in glioblastoma and non‐small cell lung cancer, its reduced expression is linked to enhanced tumor cell invasion and resistance to apoptosis through targets such as caspase‐3, TAp63, and Slug. Moreover, in renal cell carcinoma and prostate cancer, restoration of miR‐30c levels resulted in decreased tumorigenicity by counteracting hypoxia‐induced epithelial-mesenchymal transition and attenuating androgen receptor variant signaling."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond oncogenesis, miR‐30c also regulates metabolic and stress‐related pathways. It promotes adipogenesis by targeting genes such as plasminogen activator inhibitor-1 (PAI-1) and ALK2, thereby coordinating networks that modulate lipid metabolism and adipocyte differentiation. In acute kidney injury models, elevated urinary levels of miR‐30c-5p serve as an early diagnostic biomarker, while in liver fibrosis its targeting of delta-like ligand 4 (DLL4) correlates with suppressed angiogenesis and fibrotic progression. Other studies have implicated miR‐30c in governing the differentiation of vascular smooth muscle cells, influencing embryo morphokinetics, and modulating inflammatory as well as glucocorticoid receptor–mediated responses in tuberculosis and heart failure."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "20"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nThe regulatory network of miR‐30c is complex. Its biogenesis and activity can be modulated by transcription factors such as GATA3 and epitranscriptomic regulators like METTL14, while genetic polymorphisms within its precursor region may alter mature miR‐30c levels and impact cancer risk. Competing endogenous RNA (ceRNA) interactions—where lncRNAs sequester miR‐30c to de-repress targets including CCNE1, HIF3A, and CPEB4—further expand its functional repertoire, influencing key signaling pathways in ovarian, colorectal, and adenomyotic tissues. Additional direct targets include regulators such as BCL9, SOX9, ATF3, MAPK1, and GNAI2, underscoring miR‐30c’s role in feedback control of cell cycle progression, stress response, and inflammatory cascades. These multifaceted functions not only contribute to its tumor suppressor and metabolic regulatory roles but also present promising avenues for therapeutic intervention in malignancies and other chronic diseases."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "21", "end_ref": "45"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jessica Bockhorn, Rachel Dalton, Chika Nwachukwu, et al. 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