Epithelial-mesenchymal transition induced by SARS-CoV-2 required transcriptional upregulation of Snail

Yun-Ju Lai, Chi-Hong Chao, Chun-Che Liao, Te-An Lee, Jung-Mao Hsu, Wen-Cheng Chou, Jyun Wang, Hsiang-Chi Huang, Shing-Jyh Chang, Yi-Ling Lin, Chia-Wei Li*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

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.

Original languageAmerican English
Pages (from-to)2278-2290
Number of pages13
JournalAmerican journal of cancer research
Volume11
Issue number5
StatePublished - May 2021

Keywords

  • SARS-CoV-2
  • ACE2
  • TMPRSS2
  • epithelial-mesenchymal transition
  • EMT
  • spike
  • Snail
  • NF-KAPPA-B
  • CANCER METASTASIS
  • COVID-19
  • PROTEIN
  • ACTIVATION
  • INVASION
  • KINASE
  • TWIST

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