MIR17HG (MiR-17-92a-1 Cluster Host Gene)

While novel therapies such as rituximab and polatuzumab vedotin have led to improved outcomes, approximately 35% of patients eventually develop relapsed or refractory disease. Among these, miR-155 and miR-21 are particularly well studied, playing central roles in both tumor progression and remodeling of the tumor microenvironment. This review summarizes current evidence on the biological and clinical relevance of miRNAs in DLBCL, emphasizing their diagnostic and prognostic potential.

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.

These innovations hold promise for restoring cellular homeostasis in CF, Alzheimer's disease, and cancers by precisely tuning miR-17-5p expression to match disease-specific requirements. This review highlights the versatile role of miR-17-5p in diverse pathological processes and emphasizes its promise as a biomarker and therapeutic target, offering a path toward more personalized and effective treatments across multiple disease areas.

All these miRNAs were found to be associated with disease progression and/or response to therapy in one or more of the diseases under study. Therefore, studies on the value of the identified miRNA clusters in predicting disease progression and selecting therapies that may yield gains in treatment costs are warranted.

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.

The results of this study indicate that microRNA-mediated regulation of DUSP2 in hematologic and solid cancers appears to be a plausible mechanism that contributes to the dysregulation of MAP kinase signaling pathways in cancer by impairing negative feedback regulation. The data provide a solid foundation for future studies to investigate the consequences of regulation of DUSP function in cancer in more depth.

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.

Our findings revealed that the circulating exosomal miR-17-92 cluster may be used as a potential noninvasive biomarker to improve diagnostic efficiency for GC.

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.