Prognosis-related autophagy genes in female lung adenocarcinoma

Abstract

To screen the prognosis-related autophagy genes of female lung adenocarcinoma by the transcriptome data and clinical data from The Cancer Genome Atlas (TCGA) database. In this study, screen meaningful female lung adenocarcinoma differential genes in TCGA, use univariate Cox proportional regression model to select genes related to prognosis, and establish the best risk model. In this study, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes were applied for carrying out bioinformatics analysis of gene function. The gene expression and clinical data of 264 female lung adenocarcinoma patient samples were downloaded from TCGA. Twelve down-regulated genes: NRG3, DLC1, NLRC4, DAPK2, HSPB8, PPP1R15A, FOS, NRG1, PRKCQ, GRID1, MAP1LC3C, GABARAPL1. Up-regulated 15 genes: PARP1, BNIP3, P4HB, ATIC, IKBKE, ITGB4, VMP1, PTK6, EIF4EBP1, GAPDH, ATG9B, ERO1A, TMEM74, CDKN2A, BIRC5. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis showed that these genes were significantly associated with autophagy and mitochondria (animals). Multifactor Cox analysis of autophagy-related genes showed that ITGA6, ERO1A, FKBP1A, BAK1, CCR2, FADD, EDEM1, ATG10, ATG4A, DLC1, VAMP7, ST13 were identified as independent prognostic indicators. According to the multivariate Cox proportional hazard regression model, there was a significant difference in the survival rate observed between the high-risk group (n = 124) and the low-risk group (n = 126) during the 10-year follow-up ( P < .05). Univariate Cox analysis showed that tumor stage, T, M, and N stages, and risk score were all related to the survival rate of female lung adenocarcinoma patients. Multivariate Cox analysis found that autophagy-related risk scores were independent predictors, with an area under curve (AUC) value of 0.842. At last, there is autophagy genes differentially expressed among various clinicopathological parameters: ATG4A, BAK1, CCR2, DLC1, ERO1A, FKBP1A, ITGA6. The risk score can be used as an independent prognostic indicator for female patients with lung adenocarcinoma. The autophagy genes ITGA6, ERO1A, FKBP1A, BAK1, CCR2, FADD, EDEM1, ATG10, ATG4A, DLC1, VAMP7, ST13 were identified as prognostic genes in female lung adenocarcinoma, which may be the targets of treatment in the future.

Comprehensive analysis of autophagy-related gene expression profiles identified five gene biomarkers associated with immune infiltration and advanced plaques in carotid atherosclerosis

“…ITGA6, a member of the integrin family, plays a key role in the interaction between several cell types and participates in multiple biological processes, including cell proliferation and invasion [34]. Among the ATGs in female lung adenocarcinoma, there was a significant relationship between ITGA6 and its survival prognosis [35]. The present study showed that the autophagy-related gene, ITGA6, significantly increased in the progression of CAS.…”

Bioinformatics-based Investigation of Autophagy-Related Biomarkers in Heritable Ovarian Carcinoma

“…PTK6, also known as Protein Tyrosine Kinase 6, is another gene of interest that has been implicated in cancer pathogenesis [19][20][21]. Previous investigations have demonstrated the correlation between PTK6 expression and cancer stages in ovarian carcinoma, suggesting its potential as a staging biomarker for disease prognosis and management [22,23]. SERPINA1, or Serpin Family A Member 1, has been extensively studied in various cancers and is known to play a crucial role in regulating tumor growth and metastasis [24,25].…”

MiR-2779-x, a Key microRNA that is Related to the Tumorigenicity of the MDCK Cell Line

“…It has been shown that upregulation of the Bak1 protein expression level enhances the proliferation and migration of various tumour cells, including lung cancer cells[18], melanoma cells [19] and cervical cancer cells [20]. In addition, increased Bak1 protein expression is closely associated with poor prognosis of patients with non-small cell lung cancer [21]. Bak1 is expressed in tumour cells in a tissue-and time-speci c manner.…”