MIR106B (MicroRNA 106b)

Several EMT-related miRNAs show consistent associations with invasion, metastasis, peritoneal dissemination, prognosis, and chemoresistance, and many are detectable in circulation. Overall, EMT-related miRNAs orchestrate gastric cancer cell plasticity and tumor-microenvironment crosstalk and represent promising biomarker and therapeutic candidates that warrant validation in prospective, subtype-stratified, and translational studies.

While several promising biomarker candidates have been identified, the evidence base remains limited due to small sample sizes, heterogeneous methodologies, and inadequate follow-up data. Cortactin/FAK protein expression and immune signatures are the most promising but require validation in larger, well-designed prospective cohorts.

Kaplan-Meier survival analysis demonstrated that high expression of hsa-miR-15a (p=0.023) and hsa-miR-221 (p=0.048) significantly correlated with poorer overall survival, suggesting their potential prognostic values. Dysregulated expression of cell-cycle-related miRNAs, particularly hsa-miR-15a and hsa-miR-221, may contribute to CESC progression and serve as potential prognostic biomarkers.

CKMT2-AS1 exerts its tumor-suppressing function in breast cancer via sequestering miR-106b-5p and modulating MECP2 expression. Its decreased levels are linked to the unfavorable prognosis, positioning CKMT2-AS1 as a prospective indicator for prognosticating breast cancer.

A weak negative correlation between PTEN and three miRNAs, and weak positive correlations between CCND1 and miR-106b-5p and also TP53 and miR-20a-5p were observed. These findings emphasize the potential role of HPV and related biomarkers in the progression of breast cancer, indicating avenues for further research and therapeutic strategies.

Circulating miRNAs, including hsa-miR-3619-3p, hsa-miR-1290, and hsa-miR-1185-2-3p, correlated with AFP levels and disease stage, underscoring their value as non-invasive biomarkers. These findings demonstrate that integrated analysis of tissue and serum miRNAs can identify clinically relevant biomarkers and potential therapeutic targets in HCC.

Therefore, understanding the regulatory mechanisms related to MMP-2 and miRNAs will provide new insights into the molecular pathways that drive BC progression and highlight potential therapeutic targets for the management of invasion and metastasis. Hence, in this study, we aimed to elucidate the relationship between MMP-2 and miRNAs in BC.

Pathway enrichment linked these deregulated miRNAs to key oncogenic networks, particularly PI3K/AKT/mTOR, Wnt/β-catenin, and EMT regulation, demonstrating conserved molecular mechanisms shared with human BC and highlighting their potential as biomarkers in CMTs. These findings provide insights into the molecular mechanisms of CMT adenocarcinoma and suggest the potential of miRNA-based biomarkers for the diagnosis and treatment of CMTs.

Luciferase assays confirm that miR-106b-5p directly binds the 3'UTR of RBL2 and western blotting demonstrates the presence of RBL2 downregulation. Animal studies further validate the tumour-promoting role of miR-106b-5p via RBL2 suppression, which suggests its therapeutic potential.

Furthermore, PD-L1 knockout is associated with improved tumor outcomes in orthotopic mouse models. Collectively, our findings identify a non-classical function of PD-L1 and TET3 as a critical epigenetic modifier that suppresses PD-L1-mediated EMT and breast cancer stemness during metastatic progression.

Furthermore, survival analysis revealed that miR-93-5p (HR = 0.72, p = 0.0246), HCC stage (HR = 2.43, p = 0.0000113), TCF4 (HR = 0.66, p = 0.0106), DNAJB4 (HR = 1.29, p = 0.0214), MCC (HR = 1.35, p = 0.0268), and CYB5A (HR = 0.77, p = 0.0423) affect overall survival (OS). Finally, a combined prognostic model for the miRNA cluster and its target genes via the random forest approach revealed that the miR-106b/25 cluster and its interactome are significantly associated with OS (p < 0.0001), thereby providing a comprehensive understanding of the cluster and its targets in the development and progression of HCC and its use as a potential marker for HCC.

Importantly, we present the first evidence that miR-106b-5p is significantly upregulated in the myocardium in response to doxorubicin treatment, where it drives left ventricular dysfunction by targeting PR55α, a key regulator of PP2A activity...Coupling this innovation with AI-driven analysis of patient data may enable precision risk stratification, early intervention, and improved outcomes. miR-106b-5p thus emerges as a central therapeutic target and biomarker candidate for transforming the clinical management of cancer patients at risk for heart failure.