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Oral diseases

The CRISPR/Cas system inhibited the pro-oncogenic effects of alternatively spliced fibronectin extra domain A via editing the genome in salivary adenoid cystic carcinoma cells.


PMID 25684411

Abstract

To identify the association of fibronectin (FN) extra domain A (EDA) with the progression of salivary adenoid cystic carcinoma (SACC). Accordingly, the exclusion of EDA exon through the CRISPR/Cas9 system was investigated as the rescue for such pro-oncogenic splicing. SACC-83 cells were transiently transfected with plasmids containing recombinant EDA, and the cellular growth and motility were then accessed in vitro. Epithelial-mesenchymal transition (EMT) was investigated with immunohistochemistry, Western blot, and real-time PCR analysis. SACC tissues from 81 patients were used to access the associations between EDA+FN and clinical-pathological parameters. CRISPR/Cas9 plasmids containing sgRNA were designed and co-transfected into SACC-83 cells; the effects of EDA knockout on cellular growth and motility were then accessed. The recombinant EDA exhibited little effect on the proliferation of SACC cells, but significantly promoted the migration and invasion of the cells (Pxa0