MUC1-C influences cell survival in lung adenocarcinoma Calu-3 cells after SARS-CoV-2 infection |
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| Authors: | Dongbum Kim Sony Maharjan Jinsoo Kim Sangkyu Park Jeong-A Park Byoung Kwon Park Younghee Lee Hyung-Joo Kwon |
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| Institution: | 1.Institute of Medical Science, College of Medicine, Hallym University, Chuncheon 24252, Korea;2.Department of Microbiology, College of Medicine, Hallym University, Chuncheon 24252, Korea;3.Department of Biochemistry, College of Natural Sciences, Chungbuk National University, Cheongju 28644, Korea |
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| 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. |
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| Keywords: | Calu-3 Lung epithelial cancer Mucin 1 SARS-CoV-2 STAT3 |
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