Transient receptor potential vanilloid-1 (TRPV1) channels act as suppressors of the growth of glioma

被引:2
作者
Cheng, Jingjing [1 ]
Zeng, Mengliu [2 ]
Peng, Biwen [1 ]
Li, Ping
Zhao, Shiyu [3 ]
机构
[1] Wuhan Univ, Sch Basic Med Sci, Dept Physiol, Hubei Prov Key Lab Dev Originated Dis, Wuhan 430071, Peoples R China
[2] Wuhan Univ, Med Sci Res Ctr, Zhongnan Hosp, Wuhan, Peoples R China
[3] Wuhan Univ, Dept Neurosurg, Zhongnan Hosp, Wuhan, Peoples R China
关键词
Glioma; Transient receptor potential vanilloid 1; Cell apoptosis; Cell proliferation; Cell migration; CAPSAICIN INDUCES APOPTOSIS; CELL LUNG-CANCER; CALCIUM; ACTIVATION; EXPRESSION; MIGRATION; SURVIVAL; PROLIFERATION; CARCINOMA; PROMOTES;
D O I
10.1016/j.brainresbull.2024.110950
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The aim of this study was to investigate the expression and function of the transient receptor potential vanilloid 1 (TRPV1) in glioma. We found that the expression of TRPV1 mRNA and protein were upregulated in glioma compared with normal brain by qPCR and western blot analysis. In order to investigate the function of TRPV1 in glioma, short hairpin RNA (shRNA) and the inhibitor of TRPV1 were used. In vitro, the activation of TRPV1 induced cell apoptosis with decreased migration capability and inhibited proliferation, which was abolished upon TRPV1 pharmacological inhibition and silencing. Mechanistically, TRPV1 modulated glioma proliferation through the protein kinase B (Akt) signaling pathway. More importantly, in immunodeficient (NOD-SCID) mouse xenograft models, tumor size was significantly increased when TRPV1 expression was disrupted by a shRNA knockdown approach in vivo. Altogether, our findings indicate that TRPV1 negatively controls glioma cell proliferation in an Akt-dependent manner, which suggests that targeting TRPV1 may be a potential therapeutic strategy for glioma.
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页数:14
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