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STAT3 通过诱导 FOXP1 转录促进脑胶质瘤的肿瘤进展。

STAT3 promotes tumour progression in glioma by inducing FOXP1 transcription.

机构信息

National Key Clinical Specialty, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, Department of Neurosurgery, Zhujiang Hospital, Southern Medical University, Guangzhou, China.

Affiliated Bayi Brain Hospital, PLA General Army Hospital, Beijing, China.

出版信息

J Cell Mol Med. 2018 Nov;22(11):5629-5638. doi: 10.1111/jcmm.13837. Epub 2018 Aug 22.

DOI:10.1111/jcmm.13837
PMID:30134017
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6201216/
Abstract

OBJECTIVE

This paper investigated the effects of STAT3 through promoting FOXP1 transcription on proliferation, apoptosis and invasion in glioma cells.

METHODS

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.

RESULTS

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.

CONCLUSION

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.

摘要

目的

本研究旨在探讨 STAT3 通过促进 FOXP1 转录对胶质瘤细胞增殖、凋亡和侵袭的影响。

方法

采用定量实时 PCR（qRT-PCR）和 Western blot 检测评估 STAT3 和 FOXP1 在胶质瘤组织和细胞中的 mRNA 和蛋白表达水平。通过荧光素酶报告和染色质免疫沉淀（ChIP）实验确定 STAT3 和 FOXP1 之间的相关性。MTT 和集落形成实验用于鉴定细胞生长情况。流式细胞术检测胶质瘤细胞的凋亡率。Transwell 实验揭示细胞侵袭能力。

结果

STAT3 在胶质瘤组织和细胞中的 mRNA 和蛋白表达水平均升高。转染 STAT3 siRNA 后，STAT3 和 FOXP1 同时下调。STAT3 可直接调控 FOXP1 转录。STAT3 通过促进 FOXP1 转录促进胶质瘤细胞增殖、抑制细胞凋亡和增强细胞侵袭。

结论

综上所述，STAT3 基因是 FOXP1 的转录调节因子。耗尽 STAT3 可抑制胶质瘤细胞增殖和侵袭，促进细胞凋亡。STAT3 和 FOXP1 之间的这种分子机制可作为胶质瘤治疗的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6048/6201216/4f3d0222a439/JCMM-22-5629-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6048/6201216/6981754f76f3/JCMM-22-5629-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6048/6201216/88abf14868f4/JCMM-22-5629-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6048/6201216/7f5f1c5fca21/JCMM-22-5629-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6048/6201216/ce6efc6aeda0/JCMM-22-5629-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6048/6201216/793a49984c83/JCMM-22-5629-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6048/6201216/4f3d0222a439/JCMM-22-5629-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6048/6201216/6981754f76f3/JCMM-22-5629-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6048/6201216/88abf14868f4/JCMM-22-5629-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6048/6201216/7f5f1c5fca21/JCMM-22-5629-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6048/6201216/ce6efc6aeda0/JCMM-22-5629-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6048/6201216/793a49984c83/JCMM-22-5629-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6048/6201216/4f3d0222a439/JCMM-22-5629-g006.jpg

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