{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMicroRNA‑7 (miR‑7) has emerged as a pivotal regulatory molecule in normal development and homeostasis. In the developing human pancreas, miR‑7 is highly expressed in endocrine cells during fetal and adult stages and is suggested to contribute to proper islet cell differentiation and function, with further potential to guide the efficient derivation of insulin‐producing cells from pluripotent stem cells. In addition, tissue‐specific roles in wound repair and metabolic balance underscore its broader function in normal physiology and cellular stress responses."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "4"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn diverse cancer types, miR‑7 predominantly acts as a context‑dependent tumor suppressor by targeting multiple oncogenic pathways. In breast cancer, for example, miR‑7‑5p directly downregulates key regulators such as the proteasome activator REGγ and modulates EGFR‐mediated signaling, thereby impairing proliferation and survival. In glioblastoma cells, enforced miR‑7 expression inhibits both the PI3K/Akt and Raf/MEK/ERK pathways via direct targeting of PI3K and Raf‑1, while in pancreatic cancer, upregulation of miR‑7 (either by natural compounds like curcumin or via therapeutic delivery) suppresses cell growth and metastatic behavior through downregulation of targets including SET8 and by interfering with autophagy‐derived glycolysis. Similar tumor‐suppressive effects have been observed in prostate cancer (via inhibition of the stemness factor KLF4), melanoma (by targeting IRS‑2), renal cell carcinoma, gastric cancer (through its inverse relationship with EGFR expression), and even in lung cancers where miR‑7 modulates chemoresistance and radiosensitivity. Furthermore, exosomal transfer of miR‑7 from tumor‑associated macrophages to ovarian cancer cells limits metastatic potential, and studies have revealed its sequestration by oncogenic circular RNAs as a mechanism to subvert its function."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "5", "end_ref": "25"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its oncologic implications, miR‑7 also exerts crucial roles in modulating cellular stress responses, neuroprotection, and differentiation. In dopaminergic neuronal models, miR‑7 enhances glycolytic flux and increases ATP production, thereby protecting cells from mitochondrial toxins—a process mediated via repression of factors such as RelA and subsequent upregulation of glucose transporters. In osteoblasts, miR‑7 modulation affects EGFR/Akt signaling to counteract glucocorticoid‑induced cell death, while in alveolar epithelial cells it influences sodium channel expression. Moreover, its capacity to drive neural differentiation has been leveraged in both two‑dimensional and three‑dimensional stem cell culture systems, offering promising avenues for regenerative medicine in conditions such as spinal cord injury. Emerging genetic and epigenetic studies further highlight miR‑7’s potential as a noninvasive biomarker and therapeutic target across a spectrum of diseases—ranging from subtle alterations in cancer predisposition (via variants in its binding sites) to diagnostic applications in osteosarcoma and beyond."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "26", "end_ref": "38"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Mayrin Correa-Medina, Valia Bravo-Egana, Samuel Rosero, et al. 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