Transcriptional profiles and common genes link lung cancer with the development and severity of COVID-19

Nenhuma Miniatura disponível




Cury, S. S. [UNESP]
Oliveira, J. S. [UNESP]
Biagi-Júnior, C. A.O.
Silva, W. A.
Reis, P. P. [UNESP]
Cabral-Marques, O.
Hasimoto, E. N. [UNESP]
Freire, P. P. [UNESP]
Carvalho, R. F. [UNESP]

Título da Revista

ISSN da Revista

Título de Volume



Lung cancer patients with COVID-19 present an increased risk of developing severe disease and, consequently, have poor outcomes. Determining SARS-CoV-2-host interactome in lung cancer cells and tissues, infected or uninfected with SARS-CoV-2, may reveal molecular mechanisms associated with COVID-19 development and severity in lung cancer patients. Here, we integrated transcriptome data of lung tumors from patients with small- or non-small cell lung cancer (SCLC and NSCLC) and normal lung and lung cancer cells infected with SARS-CoV-2. We aimed to characterize molecular mechanisms potentially associated with COVID-19 development and severity in lung cancer patients and to predict the SARS-CoV-2-host cell interactome. We found that the gene expression profiles of lung cell lines infected with SARS-CoV-2 resemble more primary lung tumors than non-malignant lung tissues. In addition, the transcriptomic-based interactome analysis of SCLC and NSCLC revealed increased expression of cancer genes BRCA1 and CENPF, whose proteins are known or predicted to interact with the SARS-CoV-2 spike glycoprotein and helicase, respectively. We also found that TRIB3, a gene coding a putative host-SARS-CoV-2 interacting protein associated with COVID-19 infection, is co-expressed with the up-regulated genes MTHFD2, ADM2, and GPT2 in all tested conditions. Our analysis identified biological processes such as amino acid metabolism and angiogenesis and 22 host mediators of SARS-CoV-2 infection and replication that may contribute to the development and severity of COVID-19 in lung cancers.



A549, Calu-3, Host-virus interactome, NSCLC, SARS-CoV-2, SCLC

Como citar

Gene, v. 852.