Dexmedetomidine disrupts esophagus cancer tumorigenesis by modulating circ_0003340/miR-198/HMGA2 axis

This study aimed to investigate the role of DEX in esophagus cancer and its underlying mechanism. Cell Counting Kit-8 assay and 5-ethynyl-2′-deoxyuridine assays were conducted to evaluate cell proliferation. Flow cytometry analysis and transwell assay were performed for cell apoptosis and invasion. The protein levels of cleaved caspase-3, matrix metallopeptidase 9, and high mobility group AT-hook 2 (HMGA2) were assessed by western blot assay. The expression levels of circ_0003340 and microRNA-198 (miR-198) were determined by quantitative real-time PCR. Dual-luciferase reporter assay was performed to verify the interaction between miR-198 and circ_0003340 or HMGA2. Murine xenograft model was established to investigate the role of circ_0003340 and DEX in vivo. DEX exerted antitumor effects in esophagus cancer cells. DEX hindered proliferation and invasion while inducing apoptosis of esophagus cancer cells, which was abolished by circ_0003340 elevation, HMGA2 overexpression, or miR-198 silencing. miR-198 directly interacted with circ_0003340 and HMGA2 in esophagus cancer cells. Moreover, knockdown of circ_0003340 could improve the anticancer role of DEX in vivo. DEX constrained cell carcinogenesis by regulating circ_0003340/miR-198/HMGA2 axis in esophagus cancer, providing an effective clinical implication for preventing the development of the esophagus cancer by the DEX.
Source: Anti-Cancer Drugs - Category: Cancer & Oncology Tags: Pre-Clinical Reports Source Type: research