MUC1-C influences cell survival in lung adenocarcinoma Calu-3 cells after SARS-CoV-2 infection
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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)induces coronavirus disease 2019 (COVID-19) and may increasethe risk of adverse outcomes in lung cancer patients. In thisstudy, we investigated the expression and function of mucin 1(MUC1) after SARS-CoV-2 infection in the lung epithelial cancercell line Calu-3. MUC1 is a major constituent of the mucuslayer in the respiratory tract and contributes to pathogen defense. SARS-CoV-2 infection induced MUC1 C-terminal subunit(MUC1-C) expression in a STAT3 activation-dependent manner. Inhibition of MUC1-C signaling increased apoptosis-relatedprotein levels and reduced proliferation-related protein levels;however, SARS-CoV-2 replication was not affected. Together,these results suggest that increased MUC1-C expression inresponse to SARS-CoV-2 infection may trigger the growth oflung cancer cells, and COVID-19 may be a risk factor for lungcancer patients.
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)induces coronavirus disease 2019 (COVID-19) and may increasethe risk of adverse outcomes in lung cancer patients. In thisstudy, we investigated the expression and function of mucin 1(MUC1) after SARS-CoV-2 infection in the lung epithelial cancercell line Calu-3. MUC1 is a major constituent of the mucuslayer in the respiratory tract and contributes to pathogen defense. SARS-CoV-2 infection induced MUC1 C-terminal subunit(MUC1-C) expression in a STAT3 activation-dependent manner. Inhibition of MUC1-C signaling increased apoptosis-relatedprotein levels and reduced proliferation-related protein levels;however, SARS-CoV-2 replication was not affected. Together,these results suggest that increased MUC1-C expression inresponse to SARS-CoV-2 infection may trigger the growth oflung cancer cells, and COVID-19 may be a risk factor for lungcancer patients.
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