IL-17A in the tumor microenvironment of the human colorectal adenoma-carcinoma sequence

被引:66
作者
Cui, Guanglin [1 ,2 ]
Yuan, Aping [1 ,2 ]
Goll, Rasmus [2 ]
Florholmen, Jon [2 ]
机构
[1] Zhengzhou Univ, Dept Gastroenterol, Affiliated Hosp 2, Zhengzhou, Peoples R China
[2] Univ Hosp N Norway, Dept Gastroenterol & Nutr, Tromso, Norway
关键词
carcinogenesis; colorectum; interleukin-17; tumor microenvironment; INFLAMMATORY-BOWEL-DISEASE; CANCER-CELLS; COLON-CANCER; TH17; CELLS; PROMOTES ANGIOGENESIS; EXPRESSION; INTERLEUKIN-17; CYTOKINES; MUCOSA; GROWTH;
D O I
10.3109/00365521.2012.725089
中图分类号
R57 [消化系及腹部疾病];
学科分类号
100201 [内科学];
摘要
Objectives. Interleukin (IL)-17A is an important pro-inflammatory cytokine and involved in the colorectal carcinogenesis. In this study, the authors evaluated the dynamic change of IL-17A expression in the tumor microenvironment throughout the colorectal adenoma-carcinoma sequence. Materials & methods. Using quantitative real-time PCR (polymerase chain reaction) and semi-quantitative immunohistochemistry, the authors examined the expression level of IL-17A in 50 of human colorectal adenoma tissues, 50 of colorectal cancer (CRC) tissues and 15 controls. The relationship between IL-17A expression and clinicopathological parameters throughout the sequence was also evaluated. Results. The results revealed a step-up increased IL-17A mRNA level throughout the colorectal adenoma-carcinoma sequence, which began to increase in the adenomas and became even higher in the CRCs; notably, the increase of IL-17A mRNA level in the adenomatous tissues was associated with the severity of dysplasia. Immunohistochemical analysis confirmed the real-time PCR results and revealed gradually increasing IL-17A cells in both the stroma and adenomatous/cancerous epithelium. In addition, the quantitative real-time PCR result has also revealed an increased expression of TH17-stimulating factors throughout the sequence. Conclusions. IL-17A and TH17 are highly activated throughout the colorectal adenoma-carcinoma sequence.
引用
收藏
页码:1304 / 1312
页数:9
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