MIR92A1 (MicroRNA 92a-1)

Clinically, circulating miRNA panels (e.g., miR-4257, miR-6785-5p, and miR-187-5p) enhance early detection, while miR-125a-5p boosts the trastuzumab response via ERBB2 targeting...This review highlights miRNAs as pivotal regulators in gastric carcinogenesis and promising precision medicine tools. The study findings will promote the standardization of profiling methods and accelerate translational research, both of which are essential to the advancement of GC diagnostic and therapeutic strategies.

In the myoblast model system, transduction studies with exogenous miR-17-92 or miRNA-sponge expression constructs indicated that miR-17-92 is necessary but not sufficient for oncogenic transformation. Together, these findings establish a cooperative transcriptional axis in FP-RMS involving P3F and MYCN that activates MIR17HG through a distal regulatory element, thereby contributing to oncogenic behavior and uncovering a novel mechanistic vulnerability.

ITPR3, MAPK1, and MAPK8 are biomarkers for meningioma, all targeted by SMAD3. Tamoxifen could treat meningioma by affecting paraptosis pathways, offering a promising basis for targeted therapy development.

Mechanistically, the effects driven by MIR17HG were abolished by miR-372-3p overexpression, and BCL6 was identified as a direct functional target of miR-372-3p. These findings demonstrate that exosomal MIR17HG derived from hMSCs drives the differentiation of follicular helper T cells and the progression of OS via the miR-372-3p/BCL6 axis.

The functional analysis revealed pathways significantly related to cancer progression. Employing systems biology approaches with holistic insight can identify essential genes and their regulation as possibilities for further experimental testing.

Targeting the HSF1/MIR17HG/SIRT1 axis may be helpful for the treatment of colorectal cancer. We identify HSF1-mediated enhancer activity as a novel driver of MIR17HG overexpression, promoting SIRT1-dependent colorectal cancer progression.

We confirm that miR-92a-1-5p regulates proliferation and cell cycle by targeting TP53INP1 and decreases autophagy by targeting BNIP3L. Our data suggest that miR-92a-1-5p plays a role in CML progression, and its inhibition enhances imatinib anti-leukemic efficacy, making it a potential therapeutic target.

Overall, this study unveils a novel, microRNA-driven, non-genetic mechanism contributing to acquired resistance to PI3Kα inhibitors in HNSCC. Indeed, linking hyperactive c-Myc to sustain miR-17-92 expression and consequent PTEN downregulation, we also propose that targeting PTEN-dependent downstream effectors, such as PLK1, may offer a powerful therapeutic strategy for resistant HNSCC.

This present meta-analysis identified 2 SNPs in the promoter of MIR17HG (rs9588884 C > G and rs982873 T > C) may be protective factors against cancer in Chinese Han population.

Additionally, AVN A mitigated the systemic adverse effects of 5-FU. Overall, our findings demonstrate that combinatorial therapy with AVN A and 5-FU represents an appealing opportunity and highlights KDM4C/MIR17HG/GSK-3β negative feedback loop which confers therapeutically exploitable vulnerability to chemo-refractory CRC patients.

MIR17HG silencing in CCA cells leads to expression alteration of genes, which are enriched in platinum resistance-related pathways. LncRNA MIR17HG regulates platinum resistance-associated genes and promotes cisplatin resistance partially via the miR-138-5p/AKAP9 axis by inhibiting cisplatin-induced apoptosis in CCA.