MIR182 (MicroRNA 182)

Taken together, we demonstrate a direct role of EVs in subverting the immune microenvironment and altering macrophage plasticity in a manner conducive to both tumor growth and proliferation. As such, a targeted delivery of microRNA inhibitors as drugs for altering macrophage plasticity may likely achieve better therapeutic response in pancreatic tumors.

Furthermore, we identify methyltransferase-like 3 (METTL3)-dependent m6A modification as a critical regulator of circIST1 stability. Collectively, our findings uncover a novel m6A-circIST1-miR-140-3p/miR-182-HIF-1α regulatory axis that underlies metabolic reprogramming in HCC, positioning circIST1 as a promising therapeutic target for HCC metabolic intervention.

Overall, current evidence supports miRNAs as promising diagnostic, prognostic, and predictive biomarkers in cutaneous oncology. Standardized methodologies and large-scale validation remain essential for their integration into routine clinical practice.

DNA methylation and microRNA biomarkers hold strong promises for non-invasive CRC screening. Multi-marker panels demonstrate superior diagnostic accuracy and may provide a cost-effective, scalable approach for early CRC detection in resource-limited settings.

Mechanistically, miR-182-5p enhanced metastasis via ANLN and PDE4D regulation, whereas miR-203, miR-150-5p, and miR-139-5p suppressed metastasis through PDE4D, NEGR1, and ATP11A pathways, respectively. These results highlight the opposing roles of miR-182-5p and the tumor-suppressive miRNAs in CRC metastasis and suggest their potential as biomarkers and therapeutic targets.

Overall, the study highlights a probable mechanism for miRNA packaging and release in OC through EpCAM-positive exosomes, offering potential biomarkers for monitoring disease progression and relapse.

ADAMTS9-AS2 delayed docetaxel resistance by suppressing CRPC stemness and inducing ferroptosis. The use of polymeric materials targeting PCSCs offered a novel strategy to overcome CRPC chemotherapy resistance.

These findings underscore the pivotal contribution of Tiam1 upregulation to lung cancer development. Given the pivotal role of β-catenin in oncogenesis, we conclude that ABHD11-AS1-mediated sponging of miR-182-5p leads to Tiam1 upregulation and β-catenin pathway activation, thereby promoting Cr(VI)-induced pulmonary carcinogenesis.

Evaluation of miRNAs commonly deregulated between the three groups showed 14 shared upregulated miRNAs (miR-429, miR-425-5p, miR-200c-3p, miR-200c-5p, miR-200b-3p, miR-200a-3p, miR-183-5p, miR-182-5p, miR-141-5p, miR-141-3p, miR-96-5p, miR-93-5p, miR-10a-5p, miR-10a-3p) with a progressive increase in expression levels, from ovarian EMS to TL and ultimately to ECOC. The identified miRNA expression profiles associated with the progression from ovarian EMS, TL and ECOC provide valuable insights into the molecular progression from benign to malignant lesions and could represent potential biomarkers for the early detection of ECOC.

ROC curve analyses revealed strong efficacy for cfDNA (AUC 0.94), miR-182 (AUC 0.91), CYFRA21-1 (AUC 0.88), and CEA (AUC 0.87) in detecting metastatic breast cancer. Combined analysis of these biomarkers will enhance the predictive accuracy of metastatic breast cancer and clarify the relationship between biomarker profiles and the characteristics of metastatic versus nonmetastatic patients using liquid biopsy technology.

Specifically, we highlight the modulatory roles of miRNA in cancer cell survival and proliferation (miR-28, miR-30b/c), invasion and metastasis (miR-218, miR-182), neoangiogenesis (miR-29c), metabolic reprogramming (miR-124), and therapy resistance (miR-378, miR-328, miR-1244). The broad implications of miRNAs in lung cancer underline their potential real-world utility, as these entities can function as biomarkers for prognosis/diagnosis and even future therapeutic targets or agents.

Exosomal miR-182 may serve as a diagnostic marker for DCM. Bioinformatic analyses predict its potential regulation of the MAPK pathway through Taok2 targeting, although this mechanistic relationship requires experimental validation. These findings provide new perspectives for the early monitoring of DCM.