{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nmiR-342 (including its 3p and 5p isoforms) has emerged as a multifaceted tumor‐suppressive regulator in numerous cancers. In colorectal, cervical, lung, breast, hepatocellular, glioma, osteosarcoma, multiple myeloma, nasopharyngeal carcinoma, chronic myeloid leukemia, and pancreatic ductal adenocarcinoma, low endogenous levels of miR-342 are frequently associated with enhanced tumor cell proliferation, migration, invasion, and chemoresistance. Functional studies have shown that restoration or overexpression of miR-342 inhibits oncogenic pathways by directly targeting key mediators – for example, by reducing DNMT1 expression in colorectal cancer; FOXM1 in cervical cancer; SREBP-1–mediated lipogenesis in prostate cancer; AGR2 and RAP2B in non–small cell lung cancer; and MCT1 in triple‐negative breast cancer. In addition, miR-342 negatively modulates members of the NF‑κB, Wnt/β‑catenin, PI3K/Akt/mTOR, and cell cycle pathways through direct repression of factors such as IKK‑γ, TAB2, TAB3, E2F1, NAA10, and CCND1. Its ability to induce caspase-dependent apoptosis—by targeting anti-apoptotic genes like BCL2L1, MCL1, and BIRC6—is particularly evident in BRCA1-defective breast cancer cells and glioblastoma. Collectively, these findings position miR-342 as a key posttranscriptional regulator whose downregulation contributes to malignant progression and therapeutic resistance in a broad spectrum of cancer types."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "19"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its role in oncogenesis, miR-342 exerts important regulatory functions in non-malignant settings. It has been shown to directly target viral genomic regions to inhibit replication of coxsackievirus B3, thereby exerting antiviral activity. In experimental models of diabetic kidney disease, overexpression of miR-342-3p suppresses the progression of interstitial fibrosis by downregulating SOX6. In bone biology, miR-342-3p promotes osteogenic differentiation by targeting transcriptional regulators such as ATF3 and Sufu, thereby enhancing osteoblast activity and supporting fracture healing. Moreover, in cardiovascular contexts, reduced miR-342-3p levels in plasma exosomes correlate with impaired cardiomyocyte repair following myocardial infarction, while in endothelial cells of diabetic patients, miR-342-3p deficiency is associated with compromised vasculogenesis and angiogenesis through regulation of FGF11. Finally, miR-342-3p can modulate host immune responses against Mycobacterium tuberculosis by influencing the balance between apoptosis and necrosis via the SOCS6 axis. 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