Work

Characterizing the oncogenic importance and exploring gene-immune cells correlation of ACTB in human cancers.

Year: 2023

Type: article

Abstract: After cardiovascular diseases, cancer is the second deadliest malignancy in the world. The current study was launched to investigate the diagnostic and prognostic landscape of Beta-actin (ACTB) via a multi-layered bioinformatics approach. ACTB expression was analyzed and validated via UALCAN, TIMER, GENT2, GEPIA, and HPA. ACTB promoter methylation was evaluated via MREXPRES. Furthermore, ACTB prognostic values and their correlation with cancer metastasis were explored through the KM plotter and TNMplot, respectively. Then, cBioPortal, CancerSEA, Enrichr, TIMER, MuTarget, and CDT were used to analyze ACTB-related genetic alterations, transcription factors (TFS), MicroRNAs (miRNAs), chemotherapeutic drugs, and the correlation between its expression, immune cells, and different other parameters. We found that ACTB expression was remarkably higher in 24 major human cancer tissues than the normal samples. Additionally, elevated ACTB expression was associated with poorer survival and metastasis in only liver hepatocellular carcinoma (LIHC), head and neck squamous cancer (HNSC), and lung adenocarcinoma (LUAD). This implies that ACTB plays a significant role in the development and progression of LIHC, HNSC, and LUAD. Furthermore, enrichment analysis showed that ACTB-associated genes regulate different Biological Processes (BP), Molecular Functions (MF), and Kyoto Encyclopedia of Genes and Genomes (KEGG) terms. Moreover, ACTB up-regulation had interesting correlations with immune infiltration of CD4+ T, and CD8+ T, tumor purity, mutant genes, and a few other important parameters. At last, via this study, we also explored ACTB-associated clinically important expression regulators, including TFS, miRNAs, and different chemotherapeutic drugs. The results of the present study suggested that ACTB might be a potential candidate biomarker in LIHC, HNSC, and LUAD.

Source: PubMed Central