The MYC/TXNIP axis mediates NCL-Suppressed CD8+T cell immune response in lung adenocarcinoma
Dan Xiao, Tanxiu Chen, Xinlin Yu, Ying Song, Yigang Liu, Wei Yan
TL;DR
This study shows that NCL suppresses CD8+ T cell function in lung adenocarcinoma by affecting glucose metabolism through the MYC/TXNIP pathway.
Contribution
The study identifies the MYC/TXNIP axis as a novel mechanism by which NCL regulates T cell metabolism and immune evasion in lung cancer.
Findings
NCL overexpression reduces CD8+ T cell glucose metabolism and cytotoxicity.
NCL silencing enhances T cell infiltration and anti-tumor immune function.
NCL promotes tumor progression by inhibiting T cell metabolism via the MYC/TXNIP axis.
Abstract
Lung adenocarcinoma is a deadly malignancy with immune evasion playing a key role in tumor progression. Glucose metabolism is crucial for T cell function, and the nucleolar protein NCL may influence T cell glucose metabolism. This study aims to investigate NCL’s role in T cell glucose metabolism and immune evasion by lung adenocarcinoma cells. Utilizing single-cell RNA sequencing (scRNA-seq) data from the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA), we analyzed cell clustering, annotation, and prognosis. In vitro experiments involved manipulating NCL expression in CD8+ T cells to study immune function and glucose metabolism. In vivo studies using an orthotopic transplant mouse model monitored NCL’s impact on CD8+ T cell glucose metabolism and anti-tumor immune function. NCL was associated with T cell dysfunction and glucose metabolism. NCL silencing enhanced CD8+…
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Taxonomy
TopicsFerroptosis and cancer prognosis · Immune cells in cancer · RNA modifications and cancer