Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) induces coronavirus disease 2019 (COVID-19) and may increase the risk of adverse outcomes in lung cancer patients. In this study, we investigated the expression and function of mucin 1 (MUC1) after SARS-CoV-2 infection in the lung epithelial cancer cell line Calu-3. MUC1 is a major constituent of the mucus layer 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-related protein levels and reduced proliferation-related protein levels; however, SARS-CoV-2 replication was not affected. Together, these results suggest that increased MUC1-C expression in response to SARS-CoV-2 infection may trigger the growth of lung cancer cells, and COVID-19 may be a risk factor for lung cancer patients. [BMB Reports 2021; 54(8): 425-430].
【초록키워드】 COVID-19, coronavirus disease, severe acute respiratory syndrome coronavirus 2, SARS-CoV-2, Coronavirus disease 2019, coronavirus, SARS-COV-2 infection, risk, inhibition, lung cancer, risk factor, severe acute respiratory syndrome Coronavirus, adverse outcomes, MUC1, adverse outcome, Protein, pathogen, cells, respiratory tract, mucin, respiratory, expression, SARS-CoV-2 replication, Calu-3, Signaling, Cancer cells, Trigger, STAT3, acute respiratory syndrome, subunit, acute respiratory syndrome coronavirus, growth, lung cancer patients, protein level, report, protein levels, Defense, lung epithelial, investigated, reduced, contribute, induce, not affected, C-terminal, cancer cell line, 【제목키워드】 survival, lung adenocarcinoma, Calu-3 cell, Cell, influence,