Expression of IL-17A, E, and F and their receptors in human prostatic cancer: Comparison with benign prostatic hyperplasia

Liu, Yanbo; Zhao, Xiaohui; Sun, Xuemei; Li, Yongmei; Wang, Zhenjiang; Jiang, Jing; Han, Huiming; Weigao, Shen; Corrigan, Chris J.; Ying, Sun

doi:10.1002/pros.23058

Cited by 22 publications

(25 citation statements)

References 34 publications

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“…IL-17F has been characterized in different cancer entities. For example, IL-17F is significantly elevated in prostate cancer and triggers increased NF-κB signaling in B and T cells in patients with chronic lymphocytic leukemia [5, 6]. However, the roles of IL-17B, IL-17C, and IL-17D in cancer are less defined.…”

Section: Introductionmentioning

confidence: 99%

Interleukin-17A promotes tongue squamous cell carcinoma metastasis through activating miR-23b/versican pathway

et al. 2016

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Interleukin-17A (IL-17A), a proinflammatory cytokine mainly produced by T helper 17 cells, exerts protumor or antitumor effects in different cancer entities. However, the exact role of IL-17A in carcinogenesis and progression of tongue squamous cell carcinoma (TSCC) remains unclear. Here, we found that the levels of IL-17A in serum and tumor samples were significantly increased in TSCC patients and positively correlated with tumor metastasis and clinical stage. Besides, IL-17A enhanced cell migration and invasion in SCC15, a TSCC cell line. Furthermore, IL-17A inversely correlated with miR-23b expression in TSCC specimens. In vitro, NF-κB inhibited miR-23b transcription by directly binding to its promoter region. IL-17A downregulated miR-23b expression via activating NF-κB signaling pathway characterized by increasing p65 expression in the nuclear and elevating the levels of p-IKKα and p-IκBα. Overexpression of miR-23b inhibited, whereas knockdown of miR-23b promoted migration and invasion abilities of SCC15 cells. Moreover, extracellular matrix protein versican was proved to be the direct target of miR-23b through luciferase assay. IL-17A increased versican levels in vitro and knockdown of versican by siRNA inhibited SCC15 cell migration and invasion. Taken together, these results reveal a novel mechanism that IL-17A in TSCC microenvironment promotes the migration and invasion of TSCC cells through targeting miR-23b/versican pathway.

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Section: Introductionmentioning

confidence: 99%

Interleukin-17A promotes tongue squamous cell carcinoma metastasis through activating miR-23b/versican pathway

et al. 2016

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“…Our experimental data from BPH and PC tissue according to (TRAF‐6+, ASK‐1+, Raf‐1+) and (TRAF‐6+, ASK‐1+, Raf‐1−) subgroups showed that ASK‐1/MEK‐6/p38 was expressed higher in BPH than PC. Our previous studies have demonstrated the high expression of pro‐inflammatory cytokines by prostate epithelial cells [10] and several reports have shown that IL‐17 was also expressed by these cells [30]. Therefore, these findings support the hypothesis that prostate epithelial cells could initiate immune responses and inflammation under physiological and pathological conditions.…”

Section: Discussionmentioning

confidence: 69%

Immune profiling of human prostate epithelial cells determined by expression of p38/TRAF‐6/ERK MAP kinases pathways

Bouraoui

Achour

Royuela

et al. 2017

The Kaohsiung J of Med Scie

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The aim of the present work was to study the immune profiling of prostate epithelial cells by the expression of ASK‐1/p38 and Raf‐1/ERK MAP Kinases signaling pathways mediated by TRAF‐6. Immunohistochemical and Western blot analyses for TRAF‐6, ASK‐1, MEK‐6, p38, Raf‐1, MEK‐1, ERK‐1, ERK‐2 and PSA were carried out in 5 samples of normal prostate gland, 24 samples of BPH and 19 samples of PC. Immunoreaction to TRAF‐6 was found in the cytoplasm of epithelial cells of BPH and tumor cells of PC samples. For patients with the profile (TRAF‐6+), optical densities revealed a weak immunoexpression of ASK‐1 in PC compared to BPH patients. Whereas, immunoexpression to Raf‐1 was higher in PC than in BPH. According to the expression of ASK‐1 and Raf‐1, two main profiles were identified: (TRAF‐6+, ASK‐1+, Raf‐1+) and (TRAF‐6+, ASK‐1+, RAF‐1−) in both BPH and PC. In addition, ASK‐1/p38 axis expression was increased in BPH. Raf‐1/ERK signaling pathway was increased in PC samples. On the other hand, representing of individual signaling protein expression enclosing each of p38 and ERK MAP Kinases according to TRAF‐6+ showed a qualitative behavior of ASK61/p38 and Raf‐1/ERK signaling pathways and a dynamic expression of PSA associated with immune and inflammatory process. These findings suggest that prostate epithelial cell could able an immune and inflammatory setting.

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“…All the tissue slides were stained with a similar protocol as previously described [16]. Antigen retrieval was realized under high temperature and high pressure with sodium citrate solution (PH=6).…”

Section: Immunohistochemistrymentioning

confidence: 99%

Expression and location of IL-17A, E, F and their receptors in colorectal adenocarcinoma: Comparison with benign intestinal disease

Liu

Sun

Zhao

et al. 2018

Pathology - Research and Practice

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The research aimed to investigate secretion, expression and location of IL-17 relative ligands, IL-17 relative receptors, infiltrating inflammatory cells and parenchymal structural cells in colorectal cancer (CRC) compared with ulcerative colitis (UC) and benign hyperplastic polyp. 29 human intestinal tissues with CRC, 17 with UC and 7 with polyp were stained using immunohistochemistry to evaluate immunoreactivity for IL-17 family relative ligands including IL-17A, E, F and their respective relative receptors such as IL-17RA, IL-17RB and IL-17RC. At the same time the infiltration of inflammatory cells including lymphocytes, phagocytes, mast cells and neutrophils and parenchymal structural cell changes involving vascular endothelial cells and CD90 fibroblast cells were also evaluated using the same methods The immunoreactivity or positive inflammatory cells of all the sections were analyzed using professional image analysis software to determine statistical significance. The immunoreactivity for IL-17A, IL-17RA, IL-17E, IL-17RB and IL-17F showed significant decrease in CRC tissue when compared to UC (p = 0.00001. respectively). The reduction of above IL-17 relative ligands and receptors was accompanied by an obvious decrease in the number of infiltrating neutrophils and mast cells in CRC (p = 0.00001 and p = 0.007, respectively) but accompanied by a marked increase of CD31 blood vessels (p = 0.001). The immunoreactivity of IL-17A, IL-17RA, IL-17E, IL-17RB and IL-17F and the numbers of infiltrating neutrophils and mast cells showed significant decrease in CRC tissues when compared to those in polyp (p < 0.05). In contrast, the immunoreactivity of IL-17RC and the numbers of CD3 1ymphocytes were elevated in CRC when compared with those in polyp (p = 0.0001, p = 0.007, respectively). In CRC tissues, positive correlations between IL-17A, IL-17RA with CD68 macrophages were observed respectively (r = 0.621, p = 0.0001; r = 0.75, p = 0.0001). IL-17 cytokine family including ligands and their corresponding receptors were secreted and expressed by infiltrating inflammatory cells. Not only infiltrating lymphocytes but also increased blood endothelial cells were relative significantly to genesis and progression of CRC.

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Expression of IL-17A, E, and F and their receptors in human prostatic cancer: Comparison with benign prostatic hyperplasia

Abstract: Our data are compatible with hypothesis that IL-17A acting through IL-17RA, but not IL-17CR contribute to the pathogenesis of BPH and PCa. In contrast, IL-17E interacting with the IL-17BR might have an anti-tumor effect.

Cited by 22 publications

References 34 publications

Interleukin-17A promotes tongue squamous cell carcinoma metastasis through activating miR-23b/versican pathway

Interleukin-17A promotes tongue squamous cell carcinoma metastasis through activating miR-23b/versican pathway

Immune profiling of human prostate epithelial cells determined by expression of p38/TRAF‐6/ERK MAP kinases pathways

Expression and location of IL-17A, E, F and their receptors in colorectal adenocarcinoma: Comparison with benign intestinal disease

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