Open AccessIL ‐17A promotes cell migration and invasion of glioblastoma cells via activation of PI 3K/ AKT signalling pathway
Author(s) -
Zheng Qianqian,
Diao Shuo,
Wang Qi,
Zhu Chen,
Sun Xun,
Yin Bo,
Zhang Xinwen,
Meng Xin,
Wang Biao
Publication year - 2019
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.13938
Subject(s) - protein kinase b , cell migration , cancer research , signal transduction , u87 , cell culture , microbiology and biotechnology , cell growth , pi3k/akt/mtor pathway , chemistry , biology , glioblastoma , biochemistry , genetics
Glioblastomas ( GBM s) are the most common of both benign and malignant primary brain tumours, in which the inflammatory and immunologic abnormalities are involved. Interleukin‐17A ( IL ‐17A) plays an important role in various inflammatory diseases and cancers. Several recent studies revealed that the expression of IL ‐17A was overexpressed in human GBM s tissue. However, the accurate role of IL ‐17A in GBM s remains unclear. In this study, we aimed to explore the effect of IL ‐17A on cell migration and invasion of GBM s and the mechanism by which the effects occurred. We found that exogenous IL ‐17A promoted significantly cell migration and invasion abilities in two GBM s cell lines (U87 MG and U251) in a time‐dependent manner. In addition, the protein expressions of PI 3K, Akt and MMP ‐2/9 were increased in the GBM s cells challenged by IL ‐17A. Furthermore, a tight junction protein ZO ‐1 was down‐regulated but Twist and Bmi1 were up‐regulated. Treatment with a PI 3K inhibitor ( LY 294002) significantly reduced the abilities of both migration and invasion in U87 MG and U251 cells. LY 294002 treatment also attenuated the IL ‐17A causing increases of protein levels of PI 3K, AKT , MMP ‐2/9, Twist and the decreases of protein level of ZO ‐1 in the U87 MG and U251 cells. Taken together, we concluded that IL ‐17A promotes the GBM cells migration and invasion via PI 3K/ AKT signalling pathway. IL ‐17A and its related signalling pathways may be potential therapeutic targets for GBM .