MIR125 (MicroRNA 125)

These findings reveal that NaAsO2 promotes M2 macrophage polarization through the miR-125a-5p/IRF4 axis, highlighting a novel epigenetic mechanism in arsenic-associated tumor microenvironments and immune dysfunction. This study provides critical insights into targeting miR-125a-5p as a therapeutic strategy.

Apart from that, repression of miR-125b-5p significantly increased the number of late apoptotic cells while overexpression reduced the number of early apoptotic cells compared to the negative control (P < 0.05). Inhibition of miR-9-5p and miR-125b-5p exert apoptotic and/ or antiproliferative effects in KMS-28BM cells, suggesting their possible role in the treatment of MM.

Moreover, therapeutic modulation of miRNA activity through mimics or inhibitors holds future potential, though delivery and safety challenges remain. Advancing our understanding of miRNA-mediated regulation in cirrhosis could transform current diagnostic and therapeutic strategies, enabling more precise and personalized liver disease management.

&lsqb;This retracts the article DOI: 10.3892/ol.2019.11195.].

miRNAs, along with RB1 and N-MYC genes, may serve as predictive and prognostic biomarkers in retinoblastoma. While previous studies have highlighted the impact of certain miRNAs on survival and clinical outcomes, our study is limited by a small sample size and lack of strong statistical correlations. Large-scale studies are needed to validate these preliminary findings and clarify their clinical significance. Understanding the role of miRNAs in cancer biology could improve retinoblastoma mechanism insights and patient care.

Dysregulation of miR-34a, miR-15b, miR-141, miR-184, miR-19a, miR-125, and miR-let-7 were observed across several studies. More research involving human participants combined with mechanistic studies integrating mRNA target analysis would be beneficial in understanding the downstream effects of phthalate exposure on gene expression and grasping the broader biological implications.

miR-203 and miR-21 significantly downregulated odonto/osteogenic differentiation in myxoid, fibromyxoid and fibroid tissues (fold change values, respectively: miR-203: 0.57 ± 0.25, 0.38 ± 0.11, 0.21 ± 0.18; miR-21: 0.21 ± 0.14, 0.21 ± 0.13, 0.082 ± 0.14). Ultimately, utilising miRNA signatures in humans as a predictive tool will help us understand the molecular processes involved in DFSCs.

In conclusion, TPL exerted an antitumor effect on SW1353 human chondrosarcoma cells and miR‑125a‑5p served an essential role in inhibiting the tumorigenic phenotype of chondrosarcoma cells. TPL exerted its inhibitory effects on chondrosarcoma cells via upregulating miR‑125a‑5p and inhibiting the PI3K/Akt signaling pathway.

Our previous research demonstrated the role of MALAT-1 (Metastasis-associated lung adenocarcinoma transcript 1) in the formation of Erlotinib-resistant LUAD cells...In conclusion, our study reveals overexpress MALAT-1 cause the drug resistance of EGFR-TKIs in non-small cell lung cancer (NSCLC) through the MALAT-1/miR-125/Rab25 axis. These findings present a potential novel therapeutic target and perspective for the treatment of LUAD.

In addition, miR-29, miR-125, miR-126, miR-143, miR-200, miR-429, and miR-451a microRNAs were predicted, which were shown to have a role in pterygium development and disease severity. Identification of these molecular mechanisms provides insights for potential diagnostic and therapeutic strategies for pterygium.

Interestingly, miR-125 family members have been recently linked to BC formation as well, and complex interactions (competing endogenous RNA networks, or ceRNET) between this molecule and target mRNA have been described. In this review, we summarize the state-of-the-art about research on this topic.

One recent study found that the upregulation of miR-145 and the downregulation of miR-155 strongly correlated with a limited chemotherapy resistance to Cisplatin, 5-Fluorouracil, and Paclitaxel, although the mechanism(s) responsible for these observations remain unidentified. The potential involvement of these targets must be further investigated to determine how and whether mechanisms of these cellular pathways may be involved in the observed lack of chemotherapy resistance. These data may be important to design targets or treatments to reduce chemotherapy resistance and improve patient treatment outcomes.