Autophagy-related genes contribute to malignant progression and have a clinical prognostic impact in colon adenocarcinoma

xlomafota13 shared this article with you from Inoreader Autophagy-related genes contribute to malignant progression and have a clinical prognostic impact in colon adenocarcinoma Via Experimental and therapeutic medicine Exp Ther Med. 2021 Sep;22(3):932. doi: 10.3892/etm.2021.10364. Epub 2021 Jul 1. ABSTRACT Autophagy has an important role in regulating tumor cell survival. However, the roles of autophagy-related genes (ARGs) during colon adenocarcinoma (COAD) progression and their prognostic value have remained elusive. The present study aimed to identify the correlation between ARGs and the progression of COAD, as well as the prognostic significance of ARGs. The transcriptome profiles and the corresponding clinicopathological information of patients with COAD were downloaded from The Cancer Genome Atlas and Genotype-Tissue Expression databases. A list of ARGs was obtained from the Human Autophagy Database and bioinformatics analysis was performed to investigate the functions of these ARGs. Statistical analyses of these genes were performed to identify independent prognostic markers. The selected prognostic markers were then validated in 15 patients with COAD via immunohistochemistry. Differentially expressed ARGs between normal and tumor tissues were identified. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses revealed that the differentially expressed ARGs were mainly enriched in toxoplasmosis and pathways in cancer. The ATG4B, DAPK1 and SERPINA1 genes were determined to be associated with COAD progression. In addition, a risk signature was proposed that may serve as an independent prognostic marker. In conclusion, ATG4B, DAPK1 and SERPINA1 are crucial participants in tumorigenesis of COAD. The present study may promote the development of novel treatment strategies for COAD. PMID:34306201 | PMC:PMC8281215 | DOI:10.3892/etm.2021.10364 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.