Volume 29, Issue 3
DOI: 10.24205/03276716.2020.928
Effects of miR-873 Targeted Regulation of FGF5 on Gastric Cancer and Its Related Mechanism
Abstract
Objective: To clarify the role of miR-873 targeted regulation of FGF5 in gastric cancer (GC) and its related mechanism.
Methods: Cancer tissues and adjacent tissues of 54 patients with GC who came to our hospital for surgery from March 2018 to April 2019 were collected. QRT-PCR technique was used to detect mRNAs in tissues and cells, Western Blot (WB) was used to determine epithelial-mesenchymal transformation (EMT) and related apoptotic proteins, MTT to measure cell activity, and flow cytometry (FC) to monitor cell apoptosis.
Results: MiR-873 was statistically down-regulated in GC tissues, and was statistically inhibited in GC cells KATO III (P<0.01). The proliferation ability was statistically lower in miR-873-inhibitor group than in miR-NC group, and that of miR-873-mimics group was higher compared with siRNA-NC group (P<0.05). The apoptosis rate was notably lower in miR-873-inhibitor group than in NC group (P<0.001), and that in miR-873-mimics group was statistically lower compared with miR-NC group (P<0.001). Transfection of pmirGLOFGF5 MUT and miR-873 mimics had no effect on cell luciferase activity. Compared with NC group, miR-873-minics and miR-873-inhibition groups had statistically lower FGF5 expression. pcDNA3.1-FGF5 group presented statistically higher and statistically lower apoptosis rate than siRNA-NC group (P<0.001). FGF5 up-regulation led to statistically upregulated β-catenin, c-myc, vimentin, Snail and N-cadherin, and statistically inhibited Bax, Caspase-3 and E-cadherin, while simultaneous miR-144-3p overexpression reversed the EMT progression caused by up-regulation of FGF5.
Conclusion: MiR-873 is a potential therapeutic method for GC by regulating FGF5 to inhibit the proliferation and EMT of GC cells.
Keywords
miR-873, FGF5, gastric cancer, EMT, apoptotic protein, proliferation