期刊
PHARMACEUTICS
卷 14, 期 7, 页码 -出版社
MDPI
DOI: 10.3390/pharmaceutics14071382
关键词
ultrasound; CRISPR; Cas9; gene editing; epithelial-mesenchymal transition; N-cadherin
资金
- National Key Research and Development Program of China [2020YFA0908800]
- National Natural Science Foundation of China [81871376, 82071935, 81901771]
- Guangdong Innovation Platform of Translational Research for Cerebrovascular Diseases
- Science, Technology and Innovation Commission of Shenzhen Municipality [JCYJ20190812171820731, JCYJ20190807144209381]
This study demonstrated a novel strategy using ultrasound combined with biosynthetic nanobubbles (Gas Vesicles, GVs) to knock out the EMT-related Cdh2 gene through CRISPR/Cas9 gene editing, effectively inhibiting tumor invasion and metastasis.
The epithelial-mesenchymal transition (EMT), a process in which epithelial cells undergo a series of biochemical changes to acquire a mesenchymal phenotype, has been linked to tumor metastasis. Here, we present a novel strategy for knocking out the EMT-related Cdh2 gene, which encodes N-cadherin through CRISPR/Cas9-mediated gene editing by an ultrasound combined with biosynthetic nanobubbles (Gas Vesicles, GVs). Polyethyleneimine were employed as a gene delivery vector to deliver sgRNA into 4T1 cells that stably express the Cas9 protein, resulting in the stable Cdh2 gene- knockout cell lines. The Western blotting assay confirmed the absence of an N-cadherin protein in these Cdh2 gene-knockout 4T1 cell lines. Significantly reduced tumor cell migration was observed in the Cdh2 gene-knockout 4T1 cells in comparison with the wild-type cells. Our study demonstrated that an ultrasound combined with GVs could effectively mediate CRISPR/Cas9 gene editing of a Cdh2 gene to inhibit tumor invasion and metastasis.
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