STAT3 promotes tumour progression in glioma by inducing FOXP1 transcription

被引：24

作者：

Sun, Xinlin ^{[1
]}

Wang, Jihui ^{[1
]}

Huang, Min ^{[1
]}

Chen, Taoliang ^{[1
]}

Chen, Jiansheng ^{[1
]}

Zhang, Fabing ^{[1
]}

Zeng, Huijun ^{[1
]}

Xu, Zhimin ^{[2
]}

Ke, Yiquan ^{[1
]}

机构：

[1] Southern Med Univ, Zhujiang Hosp, Guangdong Prov Key Lab Brain Funct Repair & Regen, Dept Neurosurg,Natl Key Clin Specialty, Guangzhou, Guangdong, Peoples R China

[2] PLA Gen Army Hosp, Affiliated Bayi Brain Hosp, Beijing, Peoples R China

来源：

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE | 2018年 / 22卷 / 11期

基金：

中国国家自然科学基金;

关键词：

FOXP1; glioma; molecular mechanism; STAT3; transcription; B-CELL LYMPHOMA; SIGNAL TRANSDUCER; GLIOBLASTOMA-MULTIFORME; IMPROVED SURVIVAL; EXPRESSION; APOPTOSIS; OVEREXPRESSION; PROLIFERATION; INHIBITION; ACTIVATOR;

D O I：

10.1111/jcmm.13837

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Objective This paper investigated the effects of STAT3 through promoting FOXP1 transcription on proliferation, apoptosis and invasion in glioma cells. MethodsResultsQuantitative real-time PCR (qRT-PCR) and Western blot assay were administered to assess the mRNA and protein expression levels of STAT3 and FOXP1 in glioma tissues and cells, respectively. Luciferase reporter and Chromatin Immunoprecipitation (ChIP) assays were implemented to determine the correlation between STAT3 and FOXP1. MTT and colony formation assays were conducted to identify cell growth. Flow cytometry was run to detect the cell apoptosis rate of glioma cells. Transwell assays were conducted to reveal cell invasion ability. The mRNA and protein expression levels of STAT3 were highly expressed in glioma tissues and cells. After cells transfected with siRNA of STAT3, both STAT3 and FOXP1 were simultaneously downregulated. STAT3 directly regulated FOXP1 transcription. STAT3 promoted cell proliferation, inhibited cell apoptosis and enhanced cell invasion through promoting FOXP1 transcription in glioma cells. ConclusionIn summary, STAT3 gene was a transcriptional regulator of FOXP1. Depleted STAT3 restrained cell proliferation and invasion, promoted cell apoptosis in glioma cells. This molecular mechanism between STAT3 and FOXP1 can serve as a therapeutic target for glioma treatment.

引用

页码：5629 / 5638

页数：10

共 48 条

[1] The Incidence, Correlation with Tumor-Infiltrating Inflammation, and Prognosis of Phosphorylated STAT3 Expression in Human Gliomas [J].