MUC1-C influences cell survival in lung adenocarcinoma Calu-3 cells after SARS-CoV-2 infection

• Published in: BMB reports Vol. 54; no. 8; pp. 425 - 430
• Main Authors: Kim, Dongbum, Maharjan, Sony, Kim, Jinsoo, Park, Sangkyu, Park, Jeong-A, Park, Byoung Kwon, Lee, Younghee, Kwon, Hyung-Joo
• Format: Journal Article
• Language: Korean
• Published: 생화학분자생물학회 31.08.2021
• Subjects: Calu-3; Lung epithelial cancer; Mucin 1; SARS-CoV-2; STAT3; SARS-CoV-2; Lung epithelial cancer; Mucin 1; Calu-3; STAT3
• ISSN: 1976-6696; 1976-670X

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]