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This galley proof is being listed electronically before publishing the final manuscript (It's not final version).

MUC1-C influences cell survival in lung adenocarcinoma Calu-3 cells after SARS-CoV-2 infection
Dongbum Kim 1,# (Research Professor), Sony Maharjan1,# (Research Professor), Jinsoo Kim2,# (Graduate Student), Sangkyu Park3 (Post-doc), Jeong-A Park3 (Post-doc), Byoung Kwon Park1 (Research professor), Younghee Lee3 (Professor), Hyung-Joo Kwon1,2,* (Professor)
1Institute of Medical Science and 2Department of Microbiology, College of Medicine, Hallym University,
3Department of Biochemistry, College of Natural Sciences, Chungbuk National University
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.
Abstract, Accepted Manuscript(in press) [Submitted on February 5, 2021, Accepted on March 30, 2021]
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