MIR128 (MicroRNA 128)

This review summarizes the expression patterns and complex regulatory mechanisms of miR-128-3p across various cancers. A profound understanding of the significance and regulation of miR-128-3p in cancer will drive the development of innovative therapeutic strategies using this molecule for combating human cancer and immune-related disorders.

Distinct mirna signatures differentiate radiation-resistant and radiation-sensitive prostate cancer cells. Mir-20a-5p, mir-128-3p, and mir-135b-5p may contribute to radioresistance, whereas mir-23b-3p and mir-381-3p may act as radiosensitizers.

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.

Drug sensitivity prediction suggested that the EN1-high group may have reduced sensitivity to temozolomide and additional chemotherapeutic agents...EN1 is associated with glioma aggressiveness, immune microenvironmental features, and predicted chemotherapeutic response, and a putative NEAT1/miR-9-5p/miR-128-3p/EN1 axis may contribute to EN1 dysregulation. These findings identify EN1 as a promising biomarker and potential therapeutic target for improving glioma treatment.

Circulating miRNA profiling showed upregulation of inflammation-associated miRNAs (miR-21-5p, miR-150-5p, miR-142-3p, miR-363-3p), linked through bioinformatic analysis to immune dysregulation, intestinal cancer, and neurotoxicity. Overall, these results indicate that low-dose exposure to pollutant mixtures can induce subtle but biologically relevant immune and epithelial changes, emphasizing the importance of mixture-based approaches in environmental risk assessment.

The potential target genes of activin A receptor type I (Acvr1), ribosomal protein S6 kinase B1 (Rps6kb1), and transforming growth factor beta receptor type 1 (Tgfbr1) were significantly lower in the kidneys of the LPS group. EVs-derived miR-128-3p in LPS induced periodontitis may cause kidney inflammation which may be mediated by, Rps6kb1, Tgfbr1, and Acvr1.

Dual-luciferase reporter assays further confirmed the interactions among PVT1, miR-128, and VEGFC. Piperine may protect RPE cells by modulating the lncRNA PVT1/miR-128 signaling pathway and promoting PEDF expression.

Additionally, our in silico analysis provides a foundation for further exploration of the regulatory network involving LINC01614, miR-128 and the RAS/Map kinase signalling pathway. Overall, this study sheds light on the intricate regulatory network in astrocytoma and presents promising avenues for the development of targeted therapies for this devastating disease.

Additionally, hsa-miR-128-3p was identified as an upstream regulator of TMBIM6. These findings highlight TMBIM6's potential as a prognostic biomarker for glioma, offering new insights into its role in glioma progression.

NA-miR-128-3p combined with natural product Oroxin B significantly affected HCC progression by the interference with VEGF and PI3K-AKT pathways, better than using NA-miR-128-3p and Oroxin B alone. Taken together, this nanoparticle and combinative administration compensate for the shortcomings of the fragile RNA drugs and the low activity of natural products, with high prospects in HCC treatment.

Several mitomiRs like miR-1, miR-133, miR-128, and miR-21 have been reported to be involved in normal physiology, survival, and pathology. Since energy metabolism is one of the most important hallmarks of carcinogenesis and its underlying mechanism involves dysregulation of mitochondrial metabolism, we have tried to collate the importance of mitomiRs in the process of cancer energy metabolism and carcinogenesis.

Blocking PD-L1 reversed the promotion of THP-1 cell proliferation and immune escape by upregulating ZEB1. The miR-128-3p/ZEB1/PD-L1 axis is involved in regulating the proliferation and immune escape of AML cells, providing new insights into the molecular mechanism of miR-128-3p in AML and, more importantly, a new target for immunotherapy of AML.