Colon cancer-induced interleukin-35 inhibits beta-catenin-mediated pro-oncogenic activity
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Yueqiang Jiang1,*, Yanling Ma2,*, RuiChao Li1 and JianHai Sun2
1Department of Gerontology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China
2Department of Oncology, the Third People’s Hospital, Wuhan, Hubei Province, China
RuiChao Li, email: email@example.com
JianHai Sun, email: firstname.lastname@example.org
Keywords: colon cancer; IL-35; β-catenin; inhibition; metastasis
Received: May 23, 2017 Accepted: November 11, 2017 Published: December 01, 2017
The occurrence and development of colon cancer is closely related to inflammation. Therefore, this study was conducted a current retrospective research to study the effect of IL-35 (interleukin 35), a newly identified anti-infective factor, on colon cancer development. The expression of IL-35 in colon cancer samples and their adjacent normal mucosa by real-time PCR, ELISA (enzyme-linked immunosorbent assay). The effect of IL-35 on patient survival, colon cancer progression, and its effect on Wnt/β-catenine signaling pathway was also assessed. IL-35 is minimally expressed in colon cancer tissues but is highly expressed in adjacent normal tissues. The down-regulation of IL-35 was significantly associated with the American Cancer Joint Committee stage and overall survival of colon cancer patients. The overexpression of IL-35 in colon cancer cells inhibits cell migration, invasion, proliferation, colony formation and cancer stem cells by inhibiting beta-catenin. IL-35 inhibits colon neoplasms in mouse. Our results suggest that IL-35 has an inhibitory effect on the development of colon cancer as a novel prognostic indicator and potential therapeutic target.
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