Characterization of fatty acid metabolism-related lncRNAs in lung adenocarcinoma identifying potential novel prognostic targets

Abstract

Lung adenocarcinoma (LUAD), a malignant respiratory tumor with an extremely poor prognosis, has troubled the medical community all over the world. According to recent studies, fatty acid metabolism (FAM) and long non-coding RNAs (lncRNAs) regulation have shown exciting results in tumor therapy. In this study, the original LUAD patient data was obtained from the TCGA database, and 12 FAM-related lncRNAs (AL390755.1, AC105020.6, TMPO-AS1, AC016737.2, AC127070.2, LINC01281, AL589986.2, GAS6-DT, AC078993.1, LINC02198, AC007032.1, and AL021026.1) that were highly related to the progression of LUAD were finally identified through bioinformatics analysis, and a risk score model for clinical reference was constructed. The window explores the immunology and molecular mechanism of LUAD, aiming to shed the hoping light on LUAD treatment.

Machine learning-based integration develops an immunogenic cell death-derived lncRNA signature for predicting prognosis and immunotherapy response in lung adenocarcinoma

“…LINC00460 is upregulated in the LUAD group and played an important role in the control of oncogenes and tumor suppressors 51 . LINC01281 is downregulated in the LUAD group and therefore may be a prognostic factor for patients with LUAD 52 . LINC00968, upregulated in the LUAD group, is involved in the Wnt signaling pathway, which is involved in the growth, migration, and invasion of NSCLC 53 .…”

Bioinformatic analysis indicated that STARD4-AS1 might be a novel ferroptosis-related biomarker of oral squamous cell carcinoma

“…AL512274.1 was localized to the nucleus in an OSCC cell line [ 53 ]. AL589986.2 was employed in the construction of a prognostic predictive model for laryngeal cancer, cervical cancer, lung adenocarcinoma, dilated cardiomyopathy, and proliferative vitreoretinopathy [ [54] , [55] , [56] , [57] , [58] ]. LINC02154, significantly expressed in both HCC cells and patient tissues with poor overall survival, has been found to promote HCC proliferation and metastasis by augmenting SPC24 promoter activity and stimulating the PI3K/AKT signaling pathway [ 59 ].…”