By mapping miR-483 regulatory circuits across multiple diseases, we define the molecular determinants of its context-dependent activity. These findings establish miR-483 as both a diagnostic biomarker and a therapeutic target whose function is dictated by cellular context.
PD-L1 expression in a subset of cases highlights immune checkpoint inhibition as a potential therapeutic strategy. Prospective validation is warranted.
2 months ago
Retrospective data • Journal • PD(L)-1 Biomarker • IO biomarker
Priorities for validation include reporter assays, gene/protein modulation, phenotypic rescue, and in vivo testing in MP-exposed models. Collectively, our results nominate miRNAs as candidate tools to interrogate and potentially mitigate MP-associated carcinogenic mechanisms.
A nomogram centered on UTP3 yielded a 1-year AUC of 0.693. This multi-omics study establishes UTP3 as a key regulator connecting epigenetic alterations, immune suppression, and tumor progression in LIHC.
These genes likely mediate their effects by influencing immune cell infiltration, participating in immune regulation, and modulating inflammatory responses. Our findings offer new insights into drug selection and immunotherapeutic strategies for SS.
This integrative model effectively predicted 1-, 3-, and 5-year survival probabilities, thereby stratifying patients into distinct risk categories for enhanced clinical decision-making and personalized follow-up strategies. This research validates the diagnostic and prognostic utility of exosomal miRNA models in MM, emphasizing their discriminative and predictive capabilities.
Mechanistically, we uncovered a novel regulatory axis wherein miR-483-3p directly modulates a BCLAF1/PUMA/BAK1 apoptotic signaling network, highlighting its critical role in maintaining PCa cell survival. Our findings provide novel insights into the complex regulatory role of miRNA in PCa progression and offer a potential therapeutic strategy for targeting miRNA-mediated pathways in metastatic disease.
Using adrenocortical carcinoma spheroids as a model, this work demonstrates that inhibiting β-catenin signaling selectively reduces the levels of EV-derived miR-139-5p and miR-483-5p, consistent with prior findings from 2D culture studies. This platform represents a groundbreaking approach to EV profiling at the single-spheroid level, unlocking new opportunities for personalized medicine, drug discovery, and targeted therapies by enabling the analysis of cellular heterogeneity and scarce biological samples such as patient-derived organoids.
Furthermore, specific epigenetic signatures such as CDH1 promoter hypermethylation and HOTAIR overexpression are being explored as potential biomarkers for early detection and treatment response. In this chapter, we review recent advances in the epigenetic landscape of HCC and discuss their diagnostic and therapeutic implications, highlighting their potential to improve patient outcomes through personalized medicine approaches.
EGCG effectively counters resistance to molecular therapies in HCC by modulating stress-response proteins, RTK signaling, and miRNA profiles. miR-575 appears to mediate its antitumor activity, suggesting potential therapeutic value for EGCG and miR-575-based strategies in treating resistant HCC.
A single week of LCD induces swift, pathway-linked shifts in plasma exosomal miRNAs in T2D. miR-494-3p and miR-362-5p emerge as promising early biomarkers for long-term glycaemic improvement and weight reduction, respectively.
Downregulated long non-coding RNA TRPM2-AS inhibits cisplatin resistance of non-small cell lung cancer cells via activation of p53- p66shc pathway...PMID: 33577026. The Publisher apologizes for any inconvenience this may cause.