Propofol inhibits the proliferation, invasion, migration, and angiogenesis of oral squamous cell carcinoma through circ_0008898‐mediated pathway

Abstract

AbstractPropofol has been shown to inhibit oral squamous cell carcinoma (OSCC) progression. However, it is not clear whether propofol mediates OSCC progression through regulating circular RNA (circRNA) network. Quantitative real‐time PCR was used to detect circ_0008898, miR‐545‐3p, and CT10 regulator of kinase‐like protein (CRKL) expression. Cell functions were determined using CCK8 assay, Edu staining, MTT assay, transwell assay, wound healing assay, tube formation assay, and flow cytometry. Protein levels were examined by western blot analysis. RNA interaction was confirmed by dual‐luciferase reporter assay and RIP assay. Our data showed that propofol repressed OSCC cell proliferation, invasion, migration, angiogenesis, and promoted apoptosis. circ_0008898 was highly expressed in OSCC, and its expression could be decreased by propofol. circ_0008898 silencing aggravated the suppressive effect of propofol on OSCC progression. In the mechanism, circ_0008898 could target miR‐545‐3p to positively regulate CRKL. MiR‐545‐3p inhibitor abolished the regulation of circ_0008898 silencing on propofol‐mediated OSCC cell progression. MiR‐545‐3p inhibited the progression of propofol‐treated OSCC cells, and this effect was reversed by CRKL overexpression. Also, circ_0008898 knockdown reduced OSCC tumor growth by regulating miR‐545‐3p/CRKL. In conclusion, propofol suppressed OSCC progression, which was achieved through regulating the circ_0008898/miR‐545‐3p/CRKL axis.