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. 2017 Dec 1;9(15):11989-11998.
doi: 10.18632/oncotarget.22857. eCollection 2018 Feb 23.

Colon cancer-induced interleukin-35 inhibits beta-catenin-mediated pro-oncogenic activity

Yueqiang Jiang  1 , Yanling Ma  2 , RuiChao Li  1 , JianHai Sun  2
Affiliations

Colon cancer-induced interleukin-35 inhibits beta-catenin-mediated pro-oncogenic activity

Yueqiang Jiang et al. Oncotarget. .

Erratum in

Retraction in

Abstract

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.

Keywords: IL-35; colon cancer; inhibition; metastasis; β-catenin.

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Conflict of interest statement

CONFLICTS OF INTEREST The authors declare that there are no competing interests regarding the publication of this paper.

Figures

Figure 1
Figure 1. The concentration of IL-35 in the serum of colon cancer patient of different regional lymph node metastasis degree
Figure 2
Figure 2. Immunohistochemical map of IL-35 in colon cancer tissues and adjacent tissues (SP, ×200)
(A) the expression of IL-35 in adjacent normal tissues; (B) the expression of IL-35 in early stage of colonrectal carcinoma; (C) the expression of IL-35 in middle stage of colonic carcinoma; (D) the expression of IL-35 at the late stage of colon carcinoma.
Figure 3
Figure 3. Survival analysis on patients with colon tissues expressing high and low content of IL-35
X axis represents survival days and y axis indicates percentage of survival.
Figure 4
Figure 4. RT-PCR product of Colon26 and Colon26/IL-35 cell lines
(A) the image of the RT-PCR product of Colon26 and Colon26/IL-35 cell lines; (B) the statistic bar graph of the RT-PCR product of Colon26 and Colon26/IL-35 cell lines in (A).
Figure 5
Figure 5
(A) Photographs of representative mice and tumors. (B) Changes in tumor volume after transplantation of Colon26 and Colon26/IL-35 cell lines. X axis represents days after transduction of vector containing Colon26 into mice. Colon26: transduction with empty vector containing Colon26; Colon26/IL-35: transduction with Colon26 cell line carrying pCAGSIH cloned with IL-35 cDNA.
Figure 6
Figure 6. The protein level of β-catenin was measured by western blotting. Colon26/IL-35 and Colon26 cells were treated with 100 ng/mL rhIL-35. n = 3
*P < 0.05.
Figure 7
Figure 7. The relative expression of β-catenin in colon cancer tissues of patients with or without lymph node metastasis
Figure 8
Figure 8. Immunohistochemistry of β-catenin in colon cancer tissues of patients with or without metastasis (SP, ×200)
(A) The expression of β-catenin in colon cancer tissue of patients without lymph node metastasis; (B) The expression of β-catenin in colon cancer tissue of patients with lymph node metastasis.
See this image and copyright information in PMC

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