SNHG5 (Small Nucleolar RNA Host Gene 5)

This study provides the first evidence that SNHG5 promotes CRC liver metastasis through direct interaction with GNB2 and subsequent activation of the Wnt/β-catenin pathway. The SNHG5-GNB2 axis orchestrates a multilayered regulatory network that integrates EMT induction, immune suppression, and metabolic adaptation, highlighting its potential as a mechanistic driver and therapeutic target in metastatic CRC.

Loss of Snhg5 did not attenuate cyst formation; if anything, disease severity was mildly but not significantly exacerbated. These findings indicate that Snhg5 modulates cell-cycle control and is dispensable for kidney development and cystogenesis in collecting duct-derived cysts.

A nomogram centered on UTP3 yielded a 1-year AUC of 0.693. This multi-omics study establishes UTP3 as a key regulator connecting epigenetic alterations, immune suppression, and tumor progression in LIHC.

Overall, SNHGs may serve as molecular biomarkers and hold potential therapeutic target value. However, existing evidence is largely based on in vitro and small-sample studies, requiring further validation in clinical cohorts and functional models.

Mechanistically, proteomic profiling coupled with RNA immunoprecipitation identified CREB5 as a direct binding partner mediating SNHG15-dependent survival signaling under genotoxic stress. These results position the SNHG15-CREB5 axis as an important player governing genomic fidelity in lung adenocarcinoma, suggesting druggable targets for precision oncology approaches.

A diminished expression of miR-133a, miR-141, miR-206, and miR-1236-3p predicted a poor OS of gastric cancer. Various non-coding RNAs are associated with the prognosis of gastric cancer based on new evidence-based medical evidence, which provides a potential value for clinical diagnosis and treatment.

Overall, the present study systematically characterized the lncRNA expression profiles associated with the RES-mediated inhibition of cell proliferation, establishing lnc-SNHG15-203 as a critical mediator of the anti-OC activity of RES. The findings could help to formulate strategies for improving OC treatment.

RA alleviates CO-induced apoptosis of hippocampal neurons and oligodendrocytes, thereby reducing central nervous system injury and exerting neuroprotective effects. LncRNA SNHG15 and LINGO-1 are key molecules mediating RA-induced inhibition of neuronal apoptosis and are associated with the BDNF/TrkB pathway. These findings provide a theoretical framework for optimizing the clinical treatment of DEACMP and lay an experimental foundation for elucidating its molecular mechanisms.

Mechanically, SNHG15 may act as the ceRNA of miR-153-3p, thereby regulating the expression of its target gene KLF5. SNHG15 promotes proliferation and metastasis by sponging miR-153-3p and regulates KLF5 expression, suggesting that SNHG15 may be a potential biomarker and therapeutic target for BC.

ZMYND8 was identified as a key downstream mRNA target (AUC = 0.811), and three potential therapeutic drugs-demecolcine, piroxicam, and vorinostat-were predicted based on DSigDB screening and validated by molecular docking, with binding energies of -6.48, -7.15, and -5.39 kcal/mol, respectively. Finally, in vitro cellular assays confirmed that SNHG25 expression was elevated in COAD cell lines (p < 0.0001), and its knockdown significantly suppressed cell proliferation, migration, and invasion. This study highlights that SNHG25 is highly expressed in COAD and promotes tumor progression through multiple mechanisms, advancing research and treatment strategies for this malignancy.

LncRNA SNHG5 inhibited GC cell growth and migration by modulating the PI3K/AKT pathway via the miR-92a-3p/BTG2 axis.

High expression of SNHG15 progression cervical cancer cell proliferation, migration, and invasion by targeting the miR-200a-3p gene.