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白细胞介素-17A通过核因子κB介导的基质金属蛋白酶表达促进结肠癌细胞的迁移和侵袭。

IL-17A Promotes the Migration and Invasiveness of Colorectal Cancer Cells Through NF-κB-Mediated MMP Expression.

作者信息

Ren Hongtao, Wang Zhongwei, Zhang Shuqun, Ma Hongbing, Wang Yali, Jia Lijun, Li Yiming

机构信息

Department of Oncology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.

出版信息

Oncol Res. 2016;23(5):249-56. doi: 10.3727/096504016X14562725373716.

DOI:10.3727/096504016X14562725373716
PMID:27098148
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7838743/
Abstract

Interleukin-17A (IL-17A) plays a significant role in many inflammatory diseases and cancers. The aim of this study is to investigate the effect of IL-17A on the invasiveness of colorectal cancer. In the study, we found that IL-17A could promote the migration and invasion of colorectal cancer cells. Furthermore, after being treated with IL-17A, the expression and activity of matrix metalloproteinase 2 (MMP-2) and MMP-9 were upregulated. Moreover, the nuclear/overall fractions and DNA-binding activity of p65 and p50 were dramatically elevated by IL-17A. Pretreatment with a nuclear factor-κB (NF-κB) inhibitor (PDTC) or PI3K/AKT inhibitor (LY294002) was proven to abolish the promoting effect of IL-17A on the invasion ability of colorectal cancer cells and upregulation of MMP-2/9. In conclusion, our findings demonstrated that IL-17A could promote the invasion of colorectal cancer cells by activating the PI3K/AKT/NF-κB signaling pathway and subsequently upregulating the expression of MMP-2/9. Our results suggest that IL-17A could serve as a promising therapeutic target for colorectal cancer.

摘要

白细胞介素-17A（IL-17A）在许多炎症性疾病和癌症中发挥着重要作用。本研究旨在探讨IL-17A对结直肠癌侵袭性的影响。在该研究中，我们发现IL-17A可促进结直肠癌细胞的迁移和侵袭。此外，用IL-17A处理后，基质金属蛋白酶2（MMP-2）和MMP-9的表达及活性上调。而且，IL-17A显著提高了p65和p50的核/总蛋白比例及DNA结合活性。事实证明，用核因子κB（NF-κB）抑制剂（PDTC）或PI3K/AKT抑制剂（LY294002）预处理可消除IL-17A对结直肠癌细胞侵袭能力的促进作用以及MMP-2/9的上调。总之，我们的研究结果表明，IL-17A可通过激活PI3K/AKT/NF-κB信号通路并随后上调MMP-2/9的表达来促进结直肠癌细胞的侵袭。我们的结果表明，IL-17A有望成为结直肠癌的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ed5/7838743/f6d155af40e6/OR-23-249-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ed5/7838743/69a63311c981/OR-23-249-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ed5/7838743/7c10208805b6/OR-23-249-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ed5/7838743/7ad2bf49faf8/OR-23-249-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ed5/7838743/f6d155af40e6/OR-23-249-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ed5/7838743/69a63311c981/OR-23-249-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ed5/7838743/7c10208805b6/OR-23-249-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ed5/7838743/7ad2bf49faf8/OR-23-249-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ed5/7838743/f6d155af40e6/OR-23-249-g004.jpg

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