期刊
JOURNAL OF CELLULAR PHYSIOLOGY
卷 230, 期 7, 页码 1430-1437出版社
WILEY
DOI: 10.1002/jcp.24796
关键词
-
资金
- Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung Memorial Hospital, and Chang Gung University of Science and Technology, Chia-Yi Campus, Taiwan [CZRPG880253, CMRPF6A0073, CMRPF6C0031, CMRPG6B0271, CMRPG6C0071, CMRPG6C0011, CMRPG6C0012, CMRPG6A0163, CMRPG6B0272, CMRPG6A0012, EZRPF6C0011]
- National Science Council, Taiwan [NSC101-2622-B-255-001-CC3, NSC102-2313-B-255-002]
The CC chemokine receptor 6 (CCR6) and its ligand CCL20 are involved in human colorectal cancer (CRC) carcinogenesis and can promote the progression of CRC. In addition, interleukin-17 (IL-17), produced by a T cell subset named Th17, has been identified as an important player in inflammatory responses, and has emerged as a mediator in inflammation-associated cancer. However, the relevance of IL-17 in the development and progression of CRC still remains to be explored. This study aimed to investigate the effect of IL-17 on the cell migration of CRC cells. Human CRC HCT-116 cells were used to study the effect of IL-17 on CCR6 expression and cell migration in CRC cells. IL-17 treatment induced migration of HCT-116 cells across the Boyden chamber membrane and increased the expression level of the CCR6. Inhibition of CCR6 by small interfering RNA (siRNA) and neutralizing antibody inhibited IL-17-induced cell migration. By using specific inhibitors and short hairpin RNA (shRNA), we demonstrated that the activation of ERK and p38 pathways are critical for IL-17-induced CCR6 expression and cell migration. Promoter activity and transcription factor ELISA assays showed that IL-17 increased NF-B-DNA binding activity in HCT-116 cells. Inhibition of NF-B activation by specific inhibitors and siRNA blocked the IL-17-induced CCR6 expression. Our findings support the hypothesis that CCR6 up-regulation stimulated by IL-17 may play an active role in CRC cell migration. J. Cell. Physiol. 230: 1430-1437, 2015. (c) 2014 Wiley Periodicals, Inc., A Wiley Company
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