Effects of anlotinib on the malignant phenotype of glioma cells by mediating NF-κB signaling pathway
- VernacularTitle:安罗替尼通过调控NF-κB信号通路对脑胶质瘤细胞恶性表型的影响
- Author:
Xin LIU
1
;
Qingshan LI
1
;
Yunpeng XIE
2
;
Shenglin ZHANG
1
;
Yi DONG
1
Author Information
1. Dept. of Oncology，the Affiliated Hospital of Chengde Medical College，Hebei Chengde 067000，China
2. Dept. of Neurosurgery，the Affiliated Hospital of Chengde Medical College，Hebei Chengde 067000，China
- Publication Type:Journal Article
- Keywords:
glioma;
anlotinib;
nuclear factor-κB signaling pathway;
epithelial-mesenchymal transition
- From:
China Pharmacy
2024;35(2):192-197
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE To investigate the effects of anlotinib on the malignant phenotype of glioma cells by regulating the nuclear factor-κB （NF-κB） signaling pathway. METHODS Human glioma T98G cells were cultured in vitro， and 5-fluorouracil was used as positive control to investigate the effects of different concentrations of anlotinib （5， 10， 20 μmol/L） on the ability of proliferation， adhesion， migration and invasion， the expressions of epithelial-mesenchymal transition （EMT） related proteins [E-cadherin， N-cadherin， vimentin and fibronectin （FN）]. NF- κB signaling pathway inhibitor （BAY 11-7082） and activator （prostratin） were additionally used to verify the possible mechanism of the above effects of anlotinib. RESULTS Anlotinib with 5， 10， 20 μmol/L could significantly decrease the activity of cell proliferation （except for 5 μmol/L anlotinib group）， migration rate， and the number of adherent cells and invasive cells， could significantly up-regulate the expression of E-cadherin protein while down-regulate the expressions of N-cadherin， vimentin and FN protein （P＜0.05）； the effect of 20 μmol/L anlotinib was similar to that of positive control （P＞0.05）. Compared with 10 μmol/L anlotinib， pathway inhibitor could significantly decrease the ability of proliferation， adhesion， migration and invasion， and the expressions of N-cadherin， vimentin， FN and phosphorylated NF-κB p65 protein， while could significantly up-regulate the expression of E-cadherin protein （P＜0.05）； above indexes were reversed significantly by pathway activator （P＜0.05）. CONCLUSIONS Anlotinib may inhibit the proliferation， adhesion， migration and invasion of human glioma T98G cells， which may be associated with the inhibition of the NF-κB signaling pathway， thus inhibiting cell EMT-like processes.
