Prognostic value of palmitoylation-regulated mechanisms in glioblastoma: integrated multi-omics analysis via least absolute shrinkage and selection operator (LASSO) regression and single-cell sequencing

棕榈酰化调控机制在胶质母细胞瘤中的预后价值:基于最小绝对收缩和选择算子(LASSO)回归和单细胞测序的整合多组学分析

阅读:3

Abstract

BACKGROUND: Accumulating evidence highlights the critical role of palmitoylation in tumorigenesis, including the regulation of oncogenic signaling pathways, metabolic reprogramming, and immune evasion mechanisms. This study was designed to systematically investigate the prognostic significance of palmitoylation-related genes in glioblastoma multiforme (GBM). METHODS: Through comparative transcriptome analysis of GBM and normal brain tissues based on The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx), we identified 343 palmitoylation-related differentially expressed genes (DEGs). Subsequently, 80 candidate genes were extracted from the constructed protein-protein interaction (PPI) network. By applying the machine learning algorithm-least absolute shrinkage and selection operator (LASSO) regression combined with Kaplan-Meier (K-M) survival analysis, we identified core genes significantly associated with patients' overall survival (OS). Furthermore, single-cell RNA sequencing (scRNA-seq) analysis demonstrated that GABRB2, NCF2, and GRIN2A were enriched in critical oncogenic pathways, including MYC targets and KRAS signaling. Meanwhile, they exhibited a significantly heterogeneous expression pattern in GBM. RESULTS: Palmitoylation-related gene expression was higher in GBM tissues than in normal brain tissue. GABRB2 and GRIN2A inhibited the proliferation and migration of GBM cell lines. NCF2 promoted the proliferation and migration of GBM cell lines. CONCLUSIONS: This study was designed to systematically investigate the prognostic significance of palmitoylation-related genes in GBM. GABRB2, NCF2, and GRIN2A are expected to become new biomarkers for GBM.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。