MIR128 (MicroRNA 128)

This is the first study comparing both SAT and VAT microRNA from the same cancer patients, stratified by adiposity assessed via CT-scan, showing depot-specific miRNA regulation. Our findings indicate that VAT is prone to metabolic dysregulation, with miR-155 emerging as a potential indicator of visceral fat remodeling.

In a word, circ-RERE promotes autophagy and immune escape in AML by regulating PD-L1 expression through the miR-128-3p/ZEB1 axis, which may provide a new target for AML therapy.

Functional assays demonstrated that this regulatory circuit modulates TC cell proliferation, invasion, and metastasis in vitro and in vivo, with GAS5 acting for miR-128-3p to regulate CDKN2A expression. These findings provide a comprehensive systems-level perspective on cuproptosis-related mechanisms in TC and highlight the therapeutic promise of targeting the cuproptosis pathway and its regulatory networks in thyroid cancer management.

Our results support the role of NOTCH1 in early phases of OSCC development, with a potential contributory role in stemness, in association with AGR2, NANOG, OCT4, and SOX2, miR-150 and miR-128. These results support a complex role of NOTCH1 in carcinoma development, i.e., from oncogenic to tumor suppressor roles and stemness maintenance, not only in invasive OSCC but also in its precursor-OED.

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.