{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMIR101‐1 functions predominantly as a tumor suppressor, and its downregulation is a common event in many human cancers. Several studies have shown that loss of MIR101‐1 expression leads to overexpression of oncogenic factors such as enhancer of zeste homolog 2 (EZH2), FOS, and other epigenetic and transcriptional regulators that drive cancer progression, metastasis, and resistance to therapy. In prostate, hepatocellular, and various other carcinomas, genomic loss or functional suppression of MIR101‐1 correlates with activation of epigenetic pathways, increased cell proliferation, invasion, and a poor clinical prognosis. Moreover, MIR101‐1 can modulate critical signaling pathways including those involved in autophagy and immune responses, thereby impacting tumor cell survival and the tumor microenvironment."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "16"}]}, {"type": "t", "text": "\n \nDisruption of MIR101‐1 activity not only releases the repression of key oncogenes but also deregulates processes such as epithelial–mesenchymal transition (EMT), angiogenesis, and proteasome function. For example, in ovarian carcinoma and head and neck cancers its downregulation is linked to enhanced cancer stemness and invasive properties via upregulation of targets like CtBP2 and COX‐2, while in lung cancer and other malignancies, MIR101‐1 modulates epigenetic regulators such as DNMT3a and proteasome maturation proteins, thereby influencing both gene expression and therapeutic responses. In addition, emerging evidence indicates that MIR101‐1 plays roles in non‐oncologic pathways, including targeting transcripts involved in the regulation of CFTR in airway epithelia and modulating autophagy through control of factors such as STMN1, RAB5A, and ATG4D."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "17", "end_ref": "32"}]}, {"type": "t", "text": "\n \nFurthermore, MIR101‐1 exerts a broad regulatory influence on the tumor microenvironment and cellular homeostasis. It modulates angiogenic processes, influences endothelial responses to shear stress, and affects metabolic as well as inflammatory pathways that are central to diseases ranging from glioblastoma and breast cancer to type 1 diabetes. Restoration of MIR101‐1 expression has been shown to sensitize tumor cells to chemotherapeutic agents, reverse drug resistance by inhibiting proteasome assembly, and suppress EMT and metastatic potential. These multifaceted actions underscore the therapeutic promise of targeting MIR101‐1 activity in precision medicine approaches for diverse malignancies and other pathological conditions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "33", "end_ref": "48"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Sooryanarayana Varambally, Qi Cao, Ram-Shankar Mani, et al. 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