{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‐637 is a primate‐specific microRNA that plays important roles in normal cellular differentiation and in non‐malignant diseases. In mesenchymal stem cells, miR‐637 helps maintain the balance between adipocyte and osteoblast differentiation by directly targeting transcription factors such as Osterix, while in osteoblasts its downregulation leads to modified expression of extracellular matrix components. Moreover, miR‐637 regulates inflammatory responses by inhibiting the expression of mediators like C‐reactive protein through competition with RNA‐binding proteins. Its function extends to the vascular compartment where, by targeting CDK6 in smooth muscle cells under hypoxic conditions, miR‐637 modulates cell cycle progression. These roles, together with the observation that altered circulating miR‐637 levels correlate with conditions such as osteoporosis, atherosclerosis, carotid artery stenosis, hypertensive retinopathy, and even endothelial dysfunction induced by oxidized low‐density lipoprotein, underscore its importance as an endogenous regulator of both bone homeostasis and cardiovascular/inflammatory processes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn various cancer types—including hepatocellular carcinoma, gliomas, pancreatic cancer, papillary thyroid carcinoma, cervical and ovarian cancers, gastric cancer, melanoma, oral squamous cell carcinoma, multiple myeloma, keloids, and triple‐negative breast cancer—miR‐637 generally acts as a tumor suppressor. Its enforced expression has been shown to inhibit cell proliferation, migration, invasion, and to induce apoptosis by directly targeting key oncogenic effectors such as STAT3, Akt1, P‐REX2a, CDK6, NUPR1, HDAC4, KLK4, Apelin, CDX2, and Smad3. In many instances, the antitumor functions of miR‐637 are compromised by its sequestration through competing endogenous RNAs—including long noncoding RNAs (e.g., C5orf66‐AS1, LINC00473, HOTTIP, FAL1, LINC01234) and circular RNAs (e.g., circKIF4A, circ_0051240, circHIPK3, circ‐NOTCH1, circ_UBAP2, and circ_0017274)—which leads to the derepression of these oncogenic pathways. It is noteworthy that while most studies support a tumor‐suppressive role for miR‐637 (for example, via inhibition of STAT3 signaling in hepatocellular carcinoma or Akt1 in pancreatic cancer), at least one report suggests that in certain hepatocellular carcinoma contexts miR‐637 might promote proliferation through Akt1 regulation, highlighting the context‐dependent nature of its function."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "12", "end_ref": "29"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nEmerging studies further suggest that miR‐637 is a promising diagnostic and prognostic biomarker in a range of pathological conditions. Its antiproliferative effects in vascular smooth muscle cells contribute to its relevance in atherosclerotic disease, while novel regulatory loops involving circRNAs (such as circ_PSD3 and circLDLR) in papillary thyroid carcinoma reveal additional layers of post‐transcriptional control. Investigations in essential hypertension have highlighted miR‐637’s role in vascular function, and studies in non–small cell lung cancer further underscore its potential clinical utility. Finally, recent work in hepatocellular carcinoma implicates circ_SNX27 in modulating miR‐637 activity, suggesting that the expanding network of miR‐637 regulators may offer new therapeutic targets."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "30", "end_ref": "35"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jin-fang Zhang, Wei-ming Fu, Ming-liang He, et al. 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