{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‐141 is emerging as a pivotal regulator of cancer cell behavior. In diverse tumor types—including ovarian, nasopharyngeal, pancreatic, gastric, breast, hepatocellular, renal, head and neck, and prostate cancers—miR‐141 modulates key malignant processes such as oxidative stress responses, epithelial–mesenchymal transition (EMT), cell cycle progression, invasion, metastasis, and chemoresistance. By directly targeting critical effectors (for example, p38α, KEAP1, MAP4K4, YAP1, Tiam1, TAZ, and the EMT‐promoting transcription factors such as ZEB1), miR‐141 can function either as a tumor suppressor or an oncogene depending on the cellular context. These multifaceted effects underscore its central role in regulating signaling pathways and cytoskeletal dynamics that determine overall tumor phenotype and therapeutic responsiveness."}, {"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": "\nIn parallel, altered circulating levels of miR‐141 in body fluids have garnered attention as a promising noninvasive biomarker for cancer detection and prognosis. Clinical studies have demonstrated that aberrant miR‐141 expression in plasma, serum, urine, and even seminal fluid correlates with the presence, progression, and treatment response of colorectal, prostate, ovarian, breast, and other malignancies. When used in combination with traditional markers (for instance, prostate‐specific antigen), miR‐141 measurement may further refine patient stratification and guide clinical management."}, {"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": "\nBeyond its role in cancer, miR‐141 contributes to host–pathogen interactions and immune regulation. Studies have revealed that during viral infections the upregulation of miR‐141 facilitates a switch in protein translation by targeting key initiation factors in enterovirus infection, while in hepatitis B and C virus infections it modulates viral gene expression through suppression of host transcriptional regulators. Moreover, miR‐141 participates in neuroinflammatory and neurodegenerative contexts—notably through feed‐forward regulatory loops implicated in amyotrophic lateral sclerosis and Parkinson’s disease—and also influences immune cell recruitment in tumor‐associated inflammatory settings."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "37", "end_ref": "45"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nFinally, miR‐141 is deeply embedded within complex noncoding RNA networks that govern both physiological and pathological processes. In the context of pregnancy, aberrant miR‐141 expression has been linked to trophoblast dysfunction and altered maternal immune responses in preeclampsia, while in gastric cancer it engages in reciprocal interactions with long noncoding and circular RNAs to modulate TGF‐β signaling and other oncogenic pathways. 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