MIR342 (MicroRNA 342)

In summary, new miRNA signatures of relevance in B-AL and B-Ly could be recognized in this study. Studies in larger cohorts are required to further validate these findings.

We established the new radiotranscriptomic signatures specifically optimized for differentiating T3b stage from T2c stage by decoding stage-specific imaging-genomic crosstalk. This new approach may overcome TNM staging limitations.

The developed immune-related miRNA prognostic signature provided an accurate prediction of NPC prognosis. Additionally, the accompanying nomogram offered a practical tool for estimating patient OS, potentially aiding clinical decision-making.

Functional analysis revealed involvement in key NB pathways. Our findings demonstrate that plasma sEV-derived miRNAs represent valuable noninvasive biomarkers for neuroblastoma diagnosis and risk stratification.

This miRNA panel outperformed the World Health Organization -endorsed Xpert MTB/RIF assay, effectively identifying early-stage PTB cases without cavity formation. These findings underscore the potential of miRNA-based diagnostics as a non-invasive and highly accurate tool for differentiating PTB from LC in patients with comparable imaging presentations, addressing a critical gap in pulmonary disease management.

The ncRNA research in A-T is nascent with five studies present a miRNA dysregulation and an ATM-dependent lncRNA surge that is lost in A-T, but leave circRNAs, neuronal tissues and functional validation unexplored. Intermediate dose stress models, total and small RNA-seq under DNA damage and oxidative stress, and CRISPR rescue/knockout screens in patient derived organoids are immediate priorities for exploring the role of ncRNAs as therapeutic targets in A-T.

Larger, heterogeneous cohorts and the progression of miRNA-based therapeutic research should further validate such studies. This review highlights the potential of miRNA in translation into better outcomes in NKTCL patients.

Pien-Tze-Huang ameliorates autoimmune hepatitis by promoting hepatocyte autophagy via inhibiting miR-342-3p/mTOR signal. This study elucidates a clear molecular mechanism for PTH's therapeutic action, highlighting its potential as a targeted treatment for AIH, and the miR-342-3p/mTOR axis serves as a viable target for future anti-AIH drug design.

MiRNAs exhibit strong potential as minimally invasive biomarkers for MASLD, contributing to improved diagnosis, prognosis, and therapeutic decision-making. Their stability and role in personalized medicine underscore their clinical relevance.

Mechanistically, circ-CCND1 in EVs entered cells and bound to KDM6B, inhibiting its activation of the ELF3 gene, leading to increased miR-342-3p, which in turn suppressed KDM6B expression, forming a feedback loop that dampened pyroptosis. In conclusions, iPSC-MSC-derived EVs inhibit inflammatory cell death in colonic epithelial cells by regulating histone modification-related pathways, highlighting their potential as a novel therapeutic strategy for UC.

We identify Slc7a11, a cysteine-glutamate antiporter linked to pro-tumoral activity, as a direct miR-342-3p target, which may be at least partially responsible for TAM phenotypic reprogramming. Our findings highlight the potential of in vivo miRNA modulation as a therapeutic strategy for TAM reprogramming, offering an approach to enhance cancer immunotherapy.

Our findings suggested that a novel DNMT1/miR-342-3p/FoxM1 signal axis promotes CCSLC self-renewal and presented a potential target for the treatment of CC through suppression of CCSLC self-renewal. However, this pathway has been previously implicated in CC, as evidenced by prior studies showing miR-342-3p-mediated downregulation of FoxM1 in cervical cancer cells. Additionally, research on liver cancer further supports the involvement of miR-342-3p in suppressing FoxM1 expression. While our study contributed to this body of knowledge, we did not present a completely novel axis but reinforced the therapeutic potential of targeting the DNMT1/miR-342-3p/FoxM1 axis to suppress CCSLC self-renewal in CC treatment.