{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nNoncoding RNAs have emerged as important regulators in a variety of pathophysiological settings. For example, one study examining lung squamous cell carcinoma (LUSC) focused on a newly identified long noncoding RNA, RP11‑116G8.5, underscoring the complexity of ncRNA regulation in tumor biology and hinting at the potential for other ncRNAs to influence disease processes."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn a separate investigation into the molecular underpinnings of inflammation in epicardial adipose tissues (EAT), miR‑6870‑3p was identified as a key posttranscriptional regulator. In patients with coronary artery disease (CAD), elevated levels of miR‑6870‑3p were associated with increased expression of Toll‑like receptor 4 (TLR4) and proinflammatory mediators such as interleukin‑6, tumor necrosis factor‑α, as well as activation of downstream components including c‑Jun N‑terminal kinase (JNK) and nuclear factor kappa B (NF‑κB). Mechanistically, miR‑6870‑3p directly targets Tollip—a negative regulator of TLR signaling—thereby releasing inhibition on the JNK/NF‑κB pathways and amplifying inflammatory cytokine production in macrophages following lipopolysaccharide stimulation."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nCollectively, these findings illustrate the critical role of miR‑6870‑3p in modulating inflammatory responses by suppressing Tollip-mediated inhibition of proinflammatory signaling, a mechanism that may have broader implications beyond the inflammatory milieu—possibly extending to other pathological states where noncoding RNAs play regulatory roles. Although the study on LUSC did not directly address miR‑6870‑3p, its inclusion in the broader narrative of ncRNA function highlights the promise of future investigations to determine whether similar regulatory paradigms exist across diverse diseases."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Hongqing Li, Qing Zhao, Zhonghao Tang "}, {"type": "b", "children": [{"type": "t", "text": "LncRNA RP11-116G8.5 promotes the progression of lung squamous cell carcinoma through sponging miR-3150b-3p/miR-6870-5p to upregulate PHF12/FOXP4."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Pathol Res Pract (2021)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.prp.2021.153566"}], "href": "https://doi.org/10.1016/j.prp.2021.153566"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "34500373"}], "href": "https://pubmed.ncbi.nlm.nih.gov/34500373"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Jian-Guo Wu, Wen-Kai Yang, Hao-Zong Huang, et al. "}, {"type": "b", "children": [{"type": "t", "text": "MiRNA-6870-3p Regulates Lipopolysaccharide Induced Epicardial Adipose Tissue Inflammatory Genes via Targeting Tollip-Mediated JNK and NF-κB Signaling in Coronary Artery Disease."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Int Heart J (2022)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1536/ihj.22-163"}], "href": "https://doi.org/10.1536/ihj.22-163"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "36184551"}], "href": "https://pubmed.ncbi.nlm.nih.gov/36184551"}]}]}]}