{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMIR29C, a member of the miR‐29 family, has emerged as a multifunctional regulator in a wide spectrum of malignancies. In tumors such as nasopharyngeal carcinoma, chronic lymphocytic leukemia, melanoma, hepatocellular carcinoma, head and neck squamous cell carcinoma, lung, esophageal, prostate, gastric, colorectal, gallbladder, and glioma, MIR29C is frequently downregulated. Functionally, this loss alleviates its repression of key oncogenic pathways by directly targeting transcripts encoding extracellular matrix proteins (collagens, laminins, integrins, and matrix metalloproteinases), cell cycle regulators (cyclin E and CCND2), and metastasis‐promoting factors (TIAM1, LAMC1, and PHLDB2). These interactions culminate in the inhibition of cell proliferation, migration, invasion, angiogenesis, and metastatic dissemination, while restoration of MIR29C levels suppresses tumor growth and improves prognostic outcomes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "23"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its tumor‐suppressive function, MIR29C also plays important roles in modulating cellular metabolism, epigenetic regulation, and chemoresistance. In skeletal muscle, increased MIR29C (along with its family member MIR29A) in type 2 diabetes contributes to impaired insulin signaling and altered glucose–lipid homeostasis. In renal and endometrial pathologies—as well as in cellular senescence and cardiac aging—MIR29C influences extracellular matrix remodeling, inflammatory cytokine production, and epigenetic modifications through targeting DNA methyltransferases (DNMT3A/B) or related effectors (such as SIRT1, FOXP1/ATG14, and TTP). In glioma and pancreatic cancer models, modulation of MIR29C levels can re‐sensitize chemoresistant cells by affecting downstream targets involved in cell cycle progression and apoptosis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "24", "end_ref": "36"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMoreover, MIR29C is increasingly recognized as a valuable biomarker and effector in immunomodulation and neurodegenerative as well as other chronic disorders. In colon cancer, MIR29C functions as a direct p53 target to suppress invasion by downregulating factors such as PHLDB2, while activation of innate immune pathways (for example, via TLR3) has been shown to upregulate MIR29C, leading to promoter demethylation and the re‐expression of tumor‐suppressor genes. In gastric cancer, cytotoxic chemotherapy can induce MIR29C expression, which contributes to its anti‐metastatic effects. Finally, decreased serum levels of MIR29C have been documented in Alzheimer’s disease and diabetic nephropathy, underscoring its potential as a non‐invasive biomarker and therapeutic target in these conditions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "37", "end_ref": "40"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Srikumar Sengupta, Johan A den Boon, I-How Chen, et al. 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