LINC00996 (Long Intergenic Non-Protein Coding RNA 996)

Finally, intracellular location of LINC00996 and the relative regulatory mechanism were predicted. In conclusion, the present study constructed a prognostic risk model based on lncRNAs associated with cuproptosis in OV, which can stratify risk and predict prognosis, and explored the regulatory mechanism of LINC00996 in cuproptosis.

Finally, an immunotherapeutic cohort confirmed the value of the CRlncSig in predicting immunotherapy outcomes. The developed CRlncSig may be promising for the clinical prediction of OC patient outcomes and immunotherapeutic responses.

Our study establishes a compelling link between two extracellular vesicles-related gene signatures, prognosis, and immune infiltration in PAAD. Notably, these signatures serve as robust prognostic indicators for PAAD patients, offering valuable insights for the strategic selection of immunotherapeutic interventions.

The correlation between the predictive signature of methylation-related lncRNA and IC50 of conventional chemotherapy drugs can provide personalized chemotherapy regimens for LUAD patients. Methylation-related lncRNA signature can effectively predict DFS of patients in LUAD.

Drug sensitivity analysis and immune infiltration studies using the CIBERSORT algorithm further elucidated the potential treatment responses in different risk groups. This comprehensive evaluation underscores the significance of lncRNAs in cuproptosis and their potential as biomarkers for lung cancer prognosis and immune microenvironment.

Four lncRNAs expression in PCa cell lines was greater than that in healthy prostate cells. The au-lncRNA prognostic model has significant clinical implications in prognosis of PCa patient.

GSEC acts as an oncogenic lncRNA by interacting with miR-873-3p, modulating EGLN3 expression. This observation underscores the potential of GSEC as a diagnostic and therapeutic target for LUAD.

We further demonstrated the strong prognostic value of the risk model in MM patients receiving different regimens, especially for those with three-drug combination of bortezomib, lenalidomide, and dexamethasone (VRd) as first-line therapy. Finally, we found that down-regulation of ATP2A1-AS1 can promote cellular senescence in MM cell lines. In conclusion, the CSRLs risk model established in present study provides a novel and more accurate method for predicting MM patients' prognosis and identifies a new target for MM therapeutic intervention.