Integration of gene profile to explore the hub genes of lung adenocarcinoma

Abstract

Background: Lung cancer is a leading cause of morbidity diseases worldwide, but the key mechanisms of lung cancer remain elusive. This study aims to integrate of GSE 118370 and GSE 32863 profile and identify the key genes and pathway involved in human lung adenocarcinoma. Methods: R software (RStudio, Version info: R 3.2.3, Forrester, USA) were utilized to find the differentially expressed genes. All the differentially expressed genes were analyzed by gene ontology, kyoto encyclopedia of genes and genomes. Protein-protein interaction networks were constructed by STRING database and analyzed by Cytohubber and Module. The cancer genome atlas database was used to verification the expression of hub genes. Quantitative reverse transcription-PCR was used to verify the bio-information results. Results: Sixty-four lung adenocarcinoma and 64 adjacent normal tissues were used for integration analysis. Five hundred ninety-nine co-expression genes were locked. Biological processes mainly enriched in angiogenesis. Cellular component focused on extracellular exosome and molecular function aimed on protein disulfide isomerase activity. Cytohubber analysis showed that GNG11, FPR2, P4HB, PIK3R1, CDC20, ADCY4, TIMP1, IL6, CXC chemokine ligand (CXCL)12, and GAS6 acted as the hub genes during lung adenocarcinoma. Module analysis presented Chemokine signaling pathway was a key pathway. Quantitative reverse transcription-PCR showed that the expression level of GNG11, FPR2, PIK3R1, ADCY4, IL6, CXCL12, and GAS6 were significantly decreased and P4HB, CDC20 and TIMP1 were increased in human adenocarcinoma tissues ( P < .05). The cancer genome atlas online analysis showed GNG11 was not associated with survival. Conclusions: This study firstly reported GNG11 acting as a hub gene in adenocarcinoma. GNG11 could be used as a biomarker for human adenocarcinoma. Chemokine signaling pathway might play important roles in lung adenocarcinoma.

Tanshinone IIA suppresses the progression of lung adenocarcinoma through regulating CCNA2-CDK2 complex and AURKA/PLK1 pathway

“…Recent years, with the progress of genome research and the development of modern biotechnology, a large amount of biological data has been accumulated, which leads to the unprecedented development of bio-information analysis 16 . More and more natural product pharmacology is looking for researching direction from bioinformatics and network pharmacology.…”

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“…It has been described as a hub gene or a candidate biomarker in different cancer types. Hua et al [ 50 ] reported in their study that GNG11 acts as a hub gene in lung adenocarcinoma. Moreover, Shi et al [ 51 ] observed that GNG11 was downregulated in lung cancer, and low expression of GNG11 was associated with worse OS for female lung cancer patients who never smoked.…”

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