Abstract

Lidocaine is a conventional local anesthetic which is shown antiproliferative of colorectal cancer (CRC) in patients. MicroRNAs (miRNAs) have been consistently demonstrated to be involved in CRC, and miR-520a-3p could suppress CRC migration, promote apoptosis by targeting epidermal growth factor receptor (EGFR). However, the mechanism by which lidocaine regulated CRC proliferation and apoptosis remains unknown. In this study, quantitative RT-PCR were used to measure miR-520a-3p and EGFR expression levels, and western blotting assays ware performed to measure EGFR expression in CRC cells. Luciferase reporter assay was employed to validate the direct targeting of EGFR by miR-520a-3p. Cell proliferation and apoptosis assays ware utilized to analyze the role of lidocaine in CRC cells. The results indicated that 500 and 1000 μM lidocaine over 24 h inhibited proliferation and induced apoptosis of CRC cells. Compared with the control group, the expression of EGFR was suppressed by lidocaine (500 μM) in CRC cells. Furthermore, miR-520a-3p could directly targets EGFR in CRC cells. Lidocaine (500 μM) increased the expression of miR-520a-3p and rescued the reduction of miR-520a-3p caused by miR-520a-3p inhibitor. The results suggested that lidocaine could suppress the expression of EGFR by upregulating miR-520a-3p, and it could induce apoptosis and inhibit proliferation in CRC cells. Lidocaine may serve as potential therapeutic regimen for colorectal cancer.

Full Text
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