{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMicroRNA‐127 (miR‐127), in its −3p/−5p forms, has emerged as a critical regulator in diverse malignancies. In several cancer types—including breast, gastric, hepatocellular, ovarian, pancreatic, prostate, diffuse large B‐cell lymphoma, and Kaposi’s sarcoma—miR‐127 is frequently downregulated, and its restoration often suppresses tumor cell proliferation, migration, invasion, and overall tumor growth by directly targeting oncogenic transcripts such as BCL6, KRAS, BAG5, SETD8, PSMB5, SKP2, and others. In breast cancer, for instance, circulating miR‐127‐3p is elevated in patient plasma and may serve as an early detection marker, whereas its intracellular downregulation contributes to oncogene activation that promotes cellular senescence escape. Similarly, in gastric cancer, forced expression of miR‐127 inhibits cell cycle progression and cell migration/invasion, underscoring its tumor‐suppressive function. Notably, albeit the majority of studies support a suppressor role, context‐dependent functions have been reported – in a subset of glioblastomas, miR‐127‐3p was found to promote cell migration and invasion via targeting SEPT7, highlighting the complex, tissue‐specific regulatory network of this miRNA."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "20"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nThe expression and regulatory activity of miR‐127 are controlled by multiple mechanisms. At the transcriptional level, the miR‐433/127 cluster is highly conserved and regulated by key transcription factors such as ERRγ and its inhibitory partner SHP, while its promoter can be subject to aberrant hypermethylation in cancers, thereby leading to its silencing. In addition, several long noncoding RNAs (for example, POU3F3 in cervical cancer and FOXD3‐AS1 in lung or melanoma contexts) as well as circular RNAs (including circLGMN in glioblastoma, hsa_circ_0006732 in colorectal cancer, and hsa_circ_0008234 in cutaneous squamous cell carcinoma) can “sponge” miR‐127—sequestering and functionally inhibiting it—and consequently contribute to tumor progression by releasing its target oncogenes from repression. These layers of regulation highlight how extrinsic cues (e.g., TGFβ, p53, and c‐Jun signaling) and endogenous competing RNAs collaboratively dictate the availability and tumor‐suppressive potency of miR‐127."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "21", "end_ref": "33"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its role in oncogenesis, miR‐127 also influences non‐malignant pathophysiological processes. In joint tissues, miR‐127–mediated regulation of matrix metalloproteinases and osteopontin affects chondrocyte proliferation and may contribute to osteoarthritis pathogenesis. In models of intervertebral disc degeneration and acute tissue injury—including acute pancreatitis with lung injury—altered miR‐127 expression appears to impact extracellular matrix remodeling. Moreover, in autoimmune conditions such as lupus nephritis, downregulation of miR‐127 leads to increased JAK1 expression and consequent amplification of type I interferon signaling, thereby identifying it as a candidate for therapeutic intervention. Collectively, these multifaceted roles underscore the diagnostic and therapeutic promise of targeting miR‐127 across varied clinical settings."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "34", "end_ref": "37"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Katarina Cuk, Manuela Zucknick, Dharanija Madhavan, et al. 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