LINC01711 (Long Intergenic Non-Protein Coding RNA 1711)

The tumor-infiltrating immune cells, chemotherapeutics efficacy, and expression of immune checkpoint genes were also evaluated between the high- and low-risk groups. The prognostic signature consisting of irlncRNAs could predict the prognosis and immune landscape of patients with ICC and may provide a novel perspective for the individualized intervention in ICC.

Notably, we developed a small extracellular vesicle (sEV)-based in vivo self-assembled siRNA system for in vivo knockdown of LINC01711 and demonstrated its potential to enhance the response rate to ICIs in LUAD. Our findings underscore the pivotal role of FAP+ CAFs in driving resistance to ICIs and propose novel therapeutic strategies to overcome this obstacle.

The developed 8-lncRNA prognostic model serves as a valid biomarker for predicting LUAD prognosis and provides potential therapeutic insights. Targeting DRlncRNAs may contribute to improved prognosis and guide future therapeutic strategies.

Experimental findings revealed that LINC01711 is highly expressed in CAF-derived exosomes, which upregulate TXN via the miR-4510/NELFE axis, promoting the glycolytic pathway and subsequently increasing the proliferation, migration, and invasion potential of BRCA cells. These results shed light on a novel molecular mechanism underlying BRCA progression and suggest potential targets for therapeutic intervention.

Additionally, variations were noted in the IC50 values for key lung cancer medications such as Cisplatin, Docetaxel, and Paclitaxel. This study identified GSH metabolism-related lncRNAs as key prognostic factors in LUAD and developed a model for risk stratification. High-risk patients showed increased tumor mutation burden (TMB) and stemness, emphasizing the potential of personalized immunotherapy to improve survival outcomes.

Our findings suggest that copy number amplification-driven Linc01711 may serve as a promising prognostic predictor for GC patients and targeting Linc01711-related cholesterol metabolism pathway may be meaningful in anticancer strategies.

In addition, interference with the expression of RAP2C-AS1 suppresses the proliferation and migration of BLCA cells, and RAP2C-AS1 could affect the expression of CD274 and CTLA4, which could serve as prognostic markers and characterize the tumor microenvironment in BLCA. Overall, the model based on the 14-TERLs signature can efficiently predict the prognosis and drug treatment response in individuals with bladder cancer.

The low-risk group exhibited a more beneficial immunological profile, was less affected by RNA methylation, and was more sensitive to the majority of anti-cancer drugs, all of which indicated a better prognostic outcome. The 4 hub lncRNAs may be fundamental to studying the mechanism of anoikis in cutaneous melanoma and provide personalized therapy for salvaging drug resistance.

Hence, in this study, we developed a signature of prognostic risk-associated CRlncRNAs that could accurately predict the prognosis of KIRC patients and constructed a related ceRNA network to shed light on the mechanistic study of KIRC. LINC01711 might serve as a potential biomarker for the early diagnosis and prognosis of KIRC patients.

Cluster 2 was identified as a hot tumor with a better immune response and therapeutic effect. Our study may provide potential biomarkers for predicting prognosis in SKCM and provide personalized clinical therapy for patients based on hot and cold tumor classification.

The autophagy-related lncRNA prognostic signature established in this study could accurately predict the prognosis of TSCC patients and may be a molecular biomarker and therapeutic target.