Propofol suppresses esophageal cancer tumorigenesis by modulating circular RNA protein tyrosine kinase 2/microRNA‐134‐5p/poly ADP‐ribose polymerase 9 axis

Emerging evidence has pointed out the potential antitumor role of propofol in esophageal cancer (EC). Circular RNAs (circRNAs) have been reported as pivotal regulators in cancer development. This work explores the potential working mechanism between propofol and circular RNA protein tyrosine kinase 2 (circ-PTK2) in EC progression and chemoresistance. The cell vitality, clone formation, apoptosis, invasion, migration, tube formation capacity in EC cells after propofol treatment (0, 5, 10 or 15 µg/mL for 24 h) were determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), colony formation, flow cytometry, transwell, wound healing and tube formation assays, respectively. Propofol (0, 5, 10, or 15 µg/mL for 24 h) significantly inhibited cell vitality, clone formation, invasion, migration, tube formation capacity, and accelerated apoptosis in EC cells in vitro. The suppressive role of propofol (10 µg/mL for 24 h) in EC progression was partly overturned by circ-PTK2 overexpression, microRNA-134-5p (miR-134-5p) inhibitor, or poly ADP-ribose polymerase 9 (PARP9) overexpression. Circ-PTK2 directly interacted with miR-134-5p, and circ-PTK2 elevated PARP9 expression by its miRNA sponge role for miR-134-5p in EC cells. Propofol dramatically impeded EC tumor growth partly through reducing the circ-PTK2 level in vivo. Propofol exerted an antitumor role in EC advancement at least partly through the circ-PTK2/miR-134-5p/PARP9 axis, providing new insight into the involvement of circRNAs in propofol-mediated effect on EC progression. This study also provides evidence that circ-PTK2 could be developed as a potential therapeutic target for EC patients. This article is protected by copyright. All rights reserved.