SNHG15 (Small Nucleolar RNA Host Gene 15)

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.

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

Therefore, the editors have lost confidence in the data presented and have decided to retract the article. The authors and their affiliated institution were informed about the concerns and the decision to retract, but they remained unresponsive.

[This retracts the article DOI: 10.3892/etm.2021.10708.].

LncRNA SNHG15 may compete with COX6B1 to bind miR-30b-3p through a ceRNA mechanism to affect proliferation, migration, and invasion of lung adenocarcinoma cells.

Furthermore, SNHG15 knockdown impeded tumor growth in mice. In conclusion, m5C-methylated lncRNA SNHG15 promotes OC progression by accelerating cell proliferation and immune evasion via the miR-545-3p/PD-L1 axis, demonstrating a tumor-promoting function of SNHG15 in OC.