KMID : 0624620210540080425
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BMB Reports 2021 Volume.54 No. 8 p.425 ~ p.430
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MUC1-C influences cell survival in lung adenocarcinoma Calu-3 cells after SARS-CoV-2 infection
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Kim Dong-Bum
Maharjan Sony Kim Jin-Soo Park Sang-Kyu Park Jeong-A Park Byoung-Kwon Lee Young-Hee Kwon Hyung-Joo
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Abstract
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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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KEYWORD
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Calu-3, Lung epithelial cancer, Mucin 1, SARS-CoV-2, STAT3
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