Natural killer cell-related gene signature predicts malignancy of glioma and the survival of patients

Abstract

Background Natural killer (NK) cells-based therapies are one of the most promising strategies against cancer. The aim of this study is to investigate the natural killer cell related genes and its prognostic value in glioma. Methods The Chinese Glioma Genome Atlas (CGGA) was used to develop the natural killer cell-related signature. Risk score was built by multivariate Cox proportional hazards model. A cohort of 326 glioma samples with whole transcriptome expression data from the CGGA database was included for discovery. The Cancer Genome Atlas (TCGA) datasets was used for validation. GO and KEGG were used to reveal the biological process and function associated with the natural killer cell-related signature. We also collected the clinical pathological features of patients with gliomas to analyze the association with tumor malignancy and patients’ survival. Results We screened for NK-related genes to build a prognostic signature, and identified the risk score based on the signature. We found that NK-related risk score was independent of various clinical factors. Nature-killer cell gene expression is correlated with clinicopathological features of gliomas. Innovatively, we demonstrated the tight relation between the risk score and immune checkpoints, and found NK-related risk score combined with PD1/PDL1 patients could predict the patient outcome. Conclusion Natural killer cell-related gene signature can predict malignancy of glioma and the survival of patients, these results might provide new view for the research of glioma malignancy and individual immunotherapy.

Construction and validation of an angiogenesis-related gene expression signature associated with clinical outcome and tumor immune microenvironment in glioma

“…Furthermore, we compared the prognostic predictive abilities of 20 different risk signatures of gliomas in TCGA from published articles, including inflammatory response-related gene (IRRG) signature ( Yan et al, 2022 ), DNA damage and repair-related gene (DDRRG) signature ( Li et al, 2022c ), CXCR members signature ( He et al, 2022 ), pyroptosis-related gene signature ( Zhang M. et al, 2021b ; Chao et al, 2022 ; Yang et al, 2022 ; Zhang et al, 2022 ), ECM-related gene (ECMRG) signature ( Li et al, 2022b ), tripartite motif (TRIM) family gene signature ( Xiao et al, 2022 ), antigen presentation machinery (APM) signature ( Chen et al, 2022 ), natural killer cell-related gene (NKRG) signature ( Li C. et al, 2022a ), IL-4-related gene (IL4RG) signature ( Qi et al, 2022 ), hypoxia-related gene (HRG) signature ( Gao et al, 2021 ), S100 family-based signature ( Hu et al, 2021 ), TIME signature ( Zhang C. et al, 2021a ), focal adhesion-related gene (FARG) signature ( Li et al, 2021 ), m6A RNA methylation regulator signature ( Cong et al, 2021 ), HDAC1-related signature ( Fan et al, 2021 ), RNA-binding protein (RBP)-based signature ( Chen et al, 2021a ) and ferroptosis-related gene (FRG) signature ( Chen et al, 2021b ). The results of univariate and multivariate Cox analyses showed that our ARG signature had independent predictive ability ( p < 0.001, Table 1 ).…”

Immune characteristics and genetic markers of esophageal cancer by single-cell analysis: implications for immunotherapy

“…Most patients exhibit significant differences in response and resistance, suggesting that further analysis of the individual tissues and individual cells in tumor patients is necessary to develop specific immunotherapy strategies ( 31 ). Based on recent reports and sequencing data, immune cells can more systematically describe the molecular signatures of the immune system ( 32 - 34 ).…”

Inflammasomes driven inflammation in lung cancer revisited: a short review

“…Interestingly, inflammation can mediate cancer resistance therapy, affecting the tumor response to chemo agents and immunotherapy [10]. In this context, studies show that inflammasomes are related to chemoresistance in different carcinomas [76][77][78], including lung cancer [42]. Besides that, few studies had showed a direct correlation between lung cancer therapy resistance and inflammasome activation.…”