The putative mechanistic insights on how SARS-CoV-2 might influence the outcomes in cancer patients

Abstract

AbstractEarly evidence indicated that cancer patients are at increased risk of adverse outcomes and mortality after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. To determine the putative mechanism by which SARS-CoV-2 affects patients with cancers, we conducted a preliminary exploration at the molecular level. We collected differentially expressed proteins (DEPs) in the lung, liver, kidney, and thyroid of postmortem coronavirus disease 2019 (COVID-19) and non-COVID-19 patients from iProX database. Furthermore, we collected differentially expressed genes (DEGs) related to overall survival (OS) in lung cancer, liver cancer, kidney cancer and thyroid cancer based on the Cancer Genome Atlas (TCGA) database. We obtained the intersection of DEPs and DEGs and identified the roles of shared and remaining DEPs in corresponding cancers based on published research. Finally, we found 192, 179, 154 and 147 DEPs in lung, liver, kidney and thyroid tissues and 486, 1140, 2245 and 31 DEGs related to OS in lung cancer, liver cancer, kidney cancer and thyroid cancer, respectively. 4, 8, 6 and 0 shared genes/proteins and 48, 42, 14 and 10 remaining proteins were verified to play a role in lung cancer, liver cancer, kidney cancer and thyroid cancer, respectively. Changes in 85% (44/52), 78% (39/50), 80% (16/20) and 90% (9/10) of the verified genes/proteins, including shared and remaining genes, showed poor effects on patients with the 4 cancer types with COVID-19. In conclusion, the changes in genes/proteins caused by SARS-CoV-2 might dictate the different degrees of adverse outcomes in patients with different tumors.