{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‑211 is a melanocyte‐lineage–specific microRNA embedded in an intron of TRPM1 and transcriptionally regulated by MITF. In melanoma, reduced miR‑211 expression has been linked to enhanced invasion, metastasis, and poor prognosis. Multiple studies demonstrate that restoring miR‑211 levels in melanoma cells limits migration and invasion by directly targeting key pro‑metastatic mRNAs—including those encoding IGF2R, TGFβR2, NFAT5, KCNMA1, NUAK1, and RAB22A—and by modulating cellular adhesion, epithelial–mesenchymal transition, and metabolic reprogramming. Moreover, miR‑211 is responsive to targeted therapies (e.g. BRAF inhibitors), resulting in alterations in pigmentation and cellular behaviors that underscore its central role in melanoma plasticity and its emerging potential as a diagnostic biomarker and therapeutic target."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "12"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its critical role in melanocytic tumors, miR‑211 exerts context‑dependent functions in a broad spectrum of malignancies. In cancers such as oral squamous cell carcinoma, triple‑negative breast cancer, non‑small cell lung cancer, renal cell carcinoma, gastric cancer, cervical cancer, hepatocellular carcinoma, and thyroid cancer, aberrant miR‑211 expression contributes to altered proliferation, invasion, metastasis, and chemoresistance. In these settings, miR‑211 targets diverse transcripts—including SNAI1, SRCIN1, BIN1, CDC25B, ZEB2, CHD5, and others—to modulate oncogenic signaling pathways. Such studies indicate that, depending on the cellular context, miR‑211 can function either as a tumor suppressor or as an oncogenic driver, thereby influencing therapeutic responses and offering a promising target for molecular‐based interventions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "13", "end_ref": "34"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond cancer, miR‑211 plays multifaceted roles in normal physiology and diverse disease states. In the retinal pigment epithelium, miR‑211 (often co‑expressed with miR‑204) is essential for promoting differentiation and maintaining epithelial barrier function. Moreover, aberrant miR‑211 expression has been linked to vascular disorders—such as atherosclerosis and vascular calcification—as well as to dysregulation of angiogenic signaling. Additional investigations have uncovered roles for miR‑211 in the unfolded protein response, circadian clock regulation, autophagy, and apoptosis; for example, by modulating pancreatic β‑cell survival, mesenchymal stem cell migration, and reactive astrocyte proliferation following spinal cord injury. These insights not only illuminate the broad impact of miR‑211 on cellular homeostasis but also highlight its potential as a therapeutic target in a variety of non‑neoplastic conditions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "35", "end_ref": "49"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Carmit Levy, Mehdi Khaled, Dimitrios Iliopoulos, et al. 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