circRNA TCFL5 Promote Esophageal Cancer Progression by Modulating M2 Macrophage Polarization via the miR-543-FMNL2 Axis

Objective. The mechanism of circRNA on M2 macrophage polarization, which contributes to esophageal cancer, remains unclear. This study is aimed at clarifying the mechanism of circRNA on esophageal cancer by regulating M2 macrophage polarization. Methods. The expression of circRNA TCFL5 and miR-543 was detected by qRT-PCR. Western blot was used to detect the expression of FMNL2 and CD163. CCK-8 and transwell assay was used to detect the proliferation, migration, and invasion of Eca109 and KYSE150, respectively. Flow cytometry was used to detect the CD163 positive cells. The contents of IL-10, TGF-beta, TNF-alpha, IL-6, and IL-1 beta were detected by ELISA. A dual-luciferase reporter system was used to detect the regulation of miR-543 to circRNA TCFL5 and FMNL2. Results. 156 upregulated circRNAs and 91 downregulated circRNAs in esophageal cancer tissues were identified, and the expression of circRNA TCFL5 showed the most significant upregulation. Overexpression of circRNA TCFL5 promotes proliferation, invasion, and migration of Eca109 and KYSE150 and promotes tumor growth in vivo. circRNA TCFL5 served as a sponge of miR-543, and FMNL2 was a downstream target gene of miR-543. circRNA TCFL5 promotes cell proliferation, migration, and invasion of Eca109 and KYSE150 by modulating the miR-543/FMNL2 axis. Macrophage M2 polarization promoted proliferation, invasion, and migration of Eca109 and KYSE150 cells, and circRNA TCFL5 mediated macrophage M2 polarization by regulating the FMNL2/miR-543 axis. Conclusion. In the present study, we identified that circRNA TCFL5 was dramatically upregulated in esophageal cancer, and circRNA TCFL5 promotes esophageal cancer progression by modulating M2 macrophage polarization via the miR-543-FMNL2 axis, which provides a potential target for the treatment of esophageal cancer.