4.5 Article

Effects of IL-17A on the occurrence of lung adenocarcinoma

期刊

CANCER BIOLOGY & THERAPY
卷 12, 期 7, 页码 610-616

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TAYLOR & FRANCIS INC
DOI: 10.4161/cbt.12.7.16302

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vascular endothelial growth factor (VEGF); angiogenesis; interleukin 17 (IL-17); lung adenocarcinoma

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  1. found of the First Affiliated Clinic College of Harbin Medical University [2009Y08]
  2. Education Department of Heilongjiang Province [12511344]

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The relationship between IL-17A and cancer, whether beneficial or antagonistic, continues to be a controversial issue. In this study, effects of IL-17A on lung adenocarcinoma were investigated using lung cancer cell lines, 95D and 95C. In the presence or absence of IL-17A, cell proliferation and VEGF secretion were detected. Effects of IL-17A on capillary networks and process of angiogenesis were also evaluated. In vivo, the level of IL-17A was assayed in the serum of lung adenocarcinoma patients. At the same time, slices of adenocarcinoma tissue were analyzed for expression of IL-17A, its receptor (IL-17RA), VEGF, CD4(+)-IL-17A(+) cells and CD8(+)-IL-17A(+) cells by immunohistochemistry and immunofluorescence assays. IL-17A did not have effect on the proliferation of 95D or 95C cells, however, the elevated expression of VEGF in supernatant of 95D or 95C cells was found to be IL-17A concentration-dependent. Supernatants from 95D or 95C cells treated with IL-17A could obviously facilitate angiogenesis, compared with IL-17A absence group (p < 0.01). Higher levels of IL-17A were detected in serum of patients with lung adenocarcinoma than healthy controls (p < 0.001). Higher positive expressions of IL-17A, IL-17RA and VEGF were confirmed in lung adenocarcinoma lesion tissues compared to pericancerous normal tissues (p < 0.001). Tnc17 cells, as well as Th17 cells were found in adenocarcinoma tissue, indicating a potential role of these cells in disease. In summary, IL-17A might affect lung adenocarcinoma by promoting angiogenesis, while the role of Tnc17 cells or Th17 cells remains to be elucidated.

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