MIR92B (MicroRNA 92b)

The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 34: 2961‑2968, 2015; DOI: 10.3892/or.2015.4323].

Our study demonstrates that TUT4-mediated elevation of the miR-92b-3p/-5p ratio promotes COL7A1 transcription via silencing HDAC9 and alleviation of FOXP3 targeting, leading to collagen deposition and heightened TMZ resistance. Our results suggest that targeting miR-92b strand selection may serve as a potential therapeutic strategy for sensitizing GBM to TMZ.

LINC00673 functions as an oncogenic lncRNA in osteosarcoma by enhancing the malignant phenotype of osteosarcoma through miR-92b-3p/DUSP1 axis.

The diagnostic model achieved an AUC of 0.956, a sensitivity of 94%, and a specificity of 93% in the training cohort and an AUC of 0.985, a sensitivity of 86%, and a specificity of 97% in the validation cohort. Our findings demonstrates that plasma sEV miRNA exhibits a highly discriminative biomarker for distinguishing NCs group from early malignant lesions, making it a promising tool for auxiliary detection of early-stage LC.

THAP7-AS1 is firstly reported as a tumor suppressor in OC by targeting the miR-92b-5p/FA2H axis. Our findings suggest that THAP7-AS1 holds potential as therapeutic target in OC treatment.

This study aimed to evaluate the underlying mechanisms of decitabine (DAC) in inhibiting acute T-acute lymphoblastic leukemia (T-ALL) cell proliferation and promoting apoptosis. Animal experimental results indicated that both DAC and doxorubicin substantially decreased tumor length, width, volume, and mass; however, DAC demonstrated significantly superior efficacy in inhibiting tumor growth compared to doxorubicin. By selectively targeting the regulation of PTEN and 4EBP1, along with their associated downstream signaling pathways, DAC effectively modulated cellular proliferation, facilitated apoptotic processes, and restrained tumor growth, providing a robust theoretical foundation for clinical treatment strategies in T-ALL.

In this framework, the current review underscores the pivotal role of miRNAs in modulating cancer therapy outcomes and advocates for further research into miRNA profiling as a predictive tool to overcome drug resistance and optimize bevacizumab efficacy. Integrating miRNA analysis into clinical practice holds promise for advancing personalized cancer treatment and improving patient prognosis.

Notably, these miRNA profiles provide mechanistic insights into As-induced toxicity and demonstrate the potential to detect low-level exposure effects before overt clinical symptoms emerge. Our findings suggest that circulating miRNAs offer valuable tools for non-invasive biomonitoring of environmental toxin exposure and elucidating the molecular pathways underlying As-related health risks.

This alters PTEN's subcellular localization, promoting nuclear PTEN and reducing cytoplasmic PTEN, which in turn leads to increased RAD51 for DNA repair and activation of the PI3K-AKT-mTOR pathway for cell proliferation, contributing to doxorubicin resistance. Our study reveals a novel mechanism of doxorubicin resistance mediated by exosomal miR-92b-5p and provides potential therapeutic targets for overcoming drug resistance in AML.

Our preliminary results, albeit limited by a small sample size, highlighted a specific miRNA expression pattern able to distinguish tumoral from normal pancreatic tissue. The diagnostic performance of these miRNAs, matching with circulating miRNAs and validated in more homogeneous and large cohorts, could represent a starting point for improving the diagnostic accuracy of PanNETs.

Mechanically, augmented miR-92b-3p expression suppressed ATXN1 and CPEB3, activating the Notch signaling pathway and thereby promoting metastasis and cisplatin resistance...Our results suggest that miR-92b-3p might be an onco-miR involved in OSCC through regulating the ATXN1/CPEB3/Notch pathway. These findings provide novel insights for treating and monitoring OSCC.

PLXNC1 is a novel target exerting dual effects on GC cell proliferation and GC cell-mediated M2 polarization. EGCG derived from HDI inhibits GC cell proliferation and targets STAT3 to inhibit M2 polarization induced by PLXNC1-mediated exosomes derived from GC cells, which may be a multi-target therapeutic agent for GC cell proliferation and immune microenvironment.