期刊
AMERICAN JOURNAL OF CANCER RESEARCH
卷 11, 期 5, 页码 2278-2290出版社
E-CENTURY PUBLISHING CORP
关键词
SARS-CoV-2; ACE2; TMPRSS2; epithelial-mesenchymal transition; EMT; spike; Snail
类别
资金
- Ministry of Science and Technology [MOST 109-2314-B-001-002, MOST 109-2314-B-001-008, 109-2628-B-009-004]
- University of Massachusetts Lowell [D50210000000022]
- Academia Sinica [AS-CFII-108-102]
- Ministry of Science and Technology, Taiwan [MOST 109-3114-Y-001-001]
- Academia Sinica Core Facility and Innovative Instrument Project [AS-CFII-108-115]
The engagement of hACE2 and SARS-CoV-2 spike protein promotes virus spread, while inducing EMT phenotypic changes and stemness in breast cancer cells through Snail modulation. The spike protein S of SARS-CoV-2 is crucial in inducing EMT marker changes, and Snail upregulation is essential for the virus-mediated aggressive phenotype in cancer.
The engagement of human angiotensin-converting enzyme 2 (hACE2) and SARS-CoV-2 spike protein facilitate virus spread. Thus far, ACE2 and TMPRSS2 expression is correlated with the epithelial-mesenchymal transition (EMT) gene signature in lung cancer. However, the mechanism for SARS-CoV-2-induced EMT has not been thoroughly explored. Here, we showed that SARS-CoV-2 induces EMT phenotypic change and stemness in breast cancer cell model and subsequently identified Snail as a modulator for this regulation. The in-depth analysis identifies the spike protein (S), but not envelope (E), nucleocapsid (N), or membrane protein (M), of SARS-CoV-2 induces EMT marker changes. Suppression of Snail expression in these cells abrogates S protein-induced invasion, migration, stemness, and lung metastasis, suggesting that Snail is required for SARS-CoV-2-mediated aggressive phenotype in cancer. This study reveals an important oncogenic role of SARS-CoV-2 in triggering breast cancer metastasis through Snail upregulation.
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