Interleukin (IL)-1 beta is a member of the IL-1 family of proteins. IL-1 receptor antagonist (IL-1RA) is an agent that binds to the IL-1 receptor, preventing IL-1 from transmitting signals to cells. The present study aimed to identify the role of the IL-1 beta/1RA axis in epithelial-mesenchymal transition (EMT), cell invasion, migration, proliferation and clone formation in colorectal cancer (CRC) and to determine its underlying mechanisms of action. Significantly increased expression of both IL-1 beta and IL-1RA was identified in CRC patient data uploaded in The Cancer Genome Atlas database, and in tumor tissues when compared with matched control tissue. High expression of IL-1 beta was associated with an increased rate of overall survival and recurrence-free survival. Further research revealed that the IL-1 beta gene was co-expressed with the IL-1RA gene in tumors of CRC patients. It was additionally determined that recombinant human (rh)IL-1 beta suppressed autophagy as well as EMT in HCT-116 cells compared with control-treated cells, whereas rhIL-1RA exhibited the opposite effect. In addition, autophagy activator rapamycin (RAPA) rescued the inhibition of EMT in rhIL-1 beta-treated HCT-116 cells. Moreover, rhIL-1 beta inhibited cell invasion, migration, proliferation and colony-formation ability, when compared with a control treatment. Compared with a control treatment rhIL-1RA promoted cell invasion, migration, proliferation, but had no effect on clone formation ability. Furthermore, both rhIL-1RA and RAPA rescued inhibition of cell invasion, migration and clone formation ability in rhIL-1 beta-treated HCT-116 cells. RAPA, but not rhIL-1RA, rescue inhibited proliferation in rhIL-1 beta-treated HCT-116 cells compared with controls. In addition, it was confirmed that rhIL-1 beta inhibited the growth of subcutaneous xenografts in nude mice, when compared with control treatments. These results indicated that upregulation of the IL-1 beta/1RA axis in CRC regulated EMT, cell invasion and migration, proliferation and clone formation via autophagy.
基金：
Puxiu Medical Talents Training Program of Pudong Hospital [PX201702]
第一作者机构：[1]Fudan Univ, Pudong Med Ctr, Dept Gen Surg, Shanghai Pudong Hosp, 2800 Gongwei Rd, Shanghai 201399, Peoples R China
共同第一作者：
通讯作者：
通讯机构：[1]Fudan Univ, Pudong Med Ctr, Dept Gen Surg, Shanghai Pudong Hosp, 2800 Gongwei Rd, Shanghai 201399, Peoples R China[3]Shanghai Jiao Tong Univ, Sch Med, Dept Gen Surg, Tongren Hosp, 1111 Xianxia Rd, Shanghai 200050, Peoples R China[*1]Department of General Surgery, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, 2800 Gongwei Road, Huinan, Pudong, Shanghai 201399, P.R. China[*2]Department of General Surgery, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, 1111 Xianxia Road, Shanghai 200050, P.R. China
推荐引用方式(GB/T 7714)：
Chen Yusheng,Yang Zhou,Deng Bo,et al.Interleukin 1 beta/1RA axis in colorectal cancer regulates tumor invasion, proliferation and apoptosis via autophagy[J].ONCOLOGY REPORTS.2020,43(3):908-918.doi:10.3892/or.2020.7475.
APA：
Chen, Yusheng,Yang, Zhou,Deng, Bo,Wu, Dejun,Quan, Yingjun&Min, Zhijun.(2020).Interleukin 1 beta/1RA axis in colorectal cancer regulates tumor invasion, proliferation and apoptosis via autophagy.ONCOLOGY REPORTS,43,(3)
MLA：
Chen, Yusheng,et al."Interleukin 1 beta/1RA axis in colorectal cancer regulates tumor invasion, proliferation and apoptosis via autophagy".ONCOLOGY REPORTS 43..3(2020):908-918
