AI Article Synopsis
- The study investigates how the SARS-CoV-2 spike protein interacts with cancer cells, leading to changes that promote aggressive cancer behaviors, specifically in breast cancer models.
- Researchers found that the virus induces a process called epithelial-mesenchymal transition (EMT), which is linked to increased invasiveness and stemness in cancer cells, with Snail identified as a key player in this process.
- By blocking Snail expression, the study showed a reduction in the aggressive traits induced by the spike protein, highlighting a potential link between COVID-19 infection and breast cancer progression.
Article Abstract
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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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8167694 | PMC |
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