STAT3 promotes tumour progression in glioma by inducing FOXP1 transcription.
STAT3 promotes tumour progression in glioma by inducing FOXP1 transcription.
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STAT3通过诱导FOXP1转录促进神经胶质瘤的肿瘤进展
DOI:
10.1111/jcmm.13837
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发表时间:
2018-11
影响因子:
5.3
通讯作者:
Ke Y
中科院分区:
文献类型:
--
作者:
Sun X;Wang J;Huang M;Chen T;Chen J;Zhang F;Zeng H;Xu Z;Ke Y
This paper investigated the effects of STAT3 through promoting FOXP1 transcription on proliferation, apoptosis and invasion in glioma cells. Quantitative 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. In 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.
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影响因子:
11.2
作者:
Gomez GG;Volinia S;Croce CM;Zanca C;Li M;Emnett R;Gutmann DH;Brennan CW;Furnari FB;Cavenee WK
通讯作者:
Cavenee WK
影响因子:
4.1
作者:
Chang, Nakho;Ahn, Sun Hee;Nam, Do-Hyun
通讯作者:
Nam, Do-Hyun
影响因子:
8
作者:
Amin, HM;McDonnell, TJ;Lai, R
通讯作者:
Lai, R
DOI:
10.1158/1078-0432.ccr-09-1444
发表时间:
2009-09-01
期刊:
Clinical cancer research : an official journal of the American Association for Cancer Research
影响因子:
--
作者:
Aster J;Kutok J
通讯作者:
Kutok J
影响因子:
12.7
作者:
Claes A;Idema AJ;Wesseling P
通讯作者:
Wesseling P