Jia L.1, Jing S.1

1Department of Gastroenterology, The Third People's Hospital of Chengdu, Affiliated Hospital of Southwest Jiaotong University, Chengdu, China.

Background/Aims: IL-33 has emerged as a key role in the development of many tumors. However, its role in EAC is unknown. The aim of this study was to assess the role of IL-33 in EAC progression and uncover its therapeutic value against EAC.

Methods: Rat model of EAC with mixed reflux of gastroduodenal was established by anastomosing jejunum with esophagus. The rats in the sham group were killed 4 weeks after surgery, and the rats in the surgery group were killed 4, 10 and 16 weeks after surgery (10 rats in each group). After cardiac blood sampling, 0.5cm of the proximal ileum segment of the esophagus and anastomotic site were completely removed for detection of tissue mRNA and H&E staining. The expressions of IL-33 were measured by qRT-PCR and Western blot. Cell viability was detected by using CCK-8 assay. The migration effect of IL-33 on esophageal cancer cells was detected by wound healing and Transwell assay.

Results: After EAC modeling, the dead rats were excluded and regrouped. There were 10 rats in control group, 8 in 4w group, 9 in 10w and 16w group. Low-grade dysplasia occurred in all 6w group, high-grade dysplasia occurred in 7 rats in 10w group and 2 rats in 16w group. EAC occurred in 1 rat in 10w group and 3 rats in 16w group. The expression of IL-33 in EAC group was higher than that in the control group, and increased with the grade of pathological stage. In vitro study, the mRNA and protein level of IL-33 in esophageal cancer cells were higher than that in human esophageal epithelial cells.

Conclusion: We successfully established the rat model of EAC. The expression of IL-33 in tissue and serum was increased during the progress from low-grade dysplasia to high-grade dysplasia to EAC. IL-33 promoted proliferation and migration of EAC cells.

Keywords: Esophageal adenocarcinoma, IL-33