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下调威廉姆斯综合征转录因子(WSTF)通过抑制 PI3K/AKT 信号通路抑制脑胶质母细胞瘤细胞的生长和侵袭。

Downregulation of Williams syndrome transcription factor (WSTF) suppresses glioblastoma cell growth and invasion by inhibiting PI3K/AKT signal pathway.

机构信息

Department of Neurosurgery, The People's Hospital of Yaan, Sichuan.

出版信息

Eur J Histochem. 2021 Nov 17;65(4):3255. doi: 10.4081/ejh.2021.3255.

DOI:10.4081/ejh.2021.3255
PMID:34784707
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8611414/
Abstract

Williams syndrome transcription factor (WSTF) participates in diverse cellular processes, including tumor cell proliferation and migration. However, the function of WSTF in glioblastoma (GBM) remains unknown. Data from the Gene Expression Profiling Interactive Analysis (GEPIA) and The Cancer Genome Atlas (TCGA) datasets showed that WSTF was up-regulated in GBM tissues. Moreover, WSTF was also increased in the GBM cells. pcDNA-mediated over-expression of WSTF contributed to cell proliferation and invasion of GBM cells, while GBM cell proliferation and invasion were suppressed by shRNA-mediated silencing of WSTF. Additionally, GBM cell apoptosis was reduced by over-expression of WSTF accompanied by decrease in Bax and cleaved caspase-3, while promoted by silencing of WSTF with increase in Bax and cleaved caspase-3. Protein expression of AKT phosphorylation was enhanced by WSTF over-expression while reduced by WSTF silencing. Inhibitor of phosphatidylinositol 3 kinase attenuated WSTF over-expression-induced increase in GBM cell proliferation and invasion. In conclusion, WSTF contributed to GBM cell growth and invasion through activation of PI3K/AKT pathway.

摘要

威廉姆斯综合征转录因子(WSTF)参与多种细胞过程,包括肿瘤细胞增殖和迁移。然而,WSTF 在胶质母细胞瘤(GBM)中的功能尚不清楚。来自基因表达谱交互分析(GEPIA)和癌症基因组图谱(TCGA)数据集的数据表明,WSTF 在 GBM 组织中上调。此外,WSTF 在 GBM 细胞中也增加。pcDNA 介导的 WSTF 过表达促进 GBM 细胞的增殖和侵袭,而 shRNA 介导的 WSTF 沉默抑制 GBM 细胞的增殖和侵袭。此外,WSTF 的过表达伴随着 Bax 和 cleaved caspase-3 的减少,导致 GBM 细胞凋亡减少,而 WSTF 的沉默伴随着 Bax 和 cleaved caspase-3 的增加,促进 GBM 细胞凋亡。WSTF 过表达增强了 AKT 磷酸化的蛋白表达,而 WSTF 沉默则降低了 AKT 磷酸化的蛋白表达。磷脂酰肌醇 3 激酶抑制剂减弱了 WSTF 过表达诱导的 GBM 细胞增殖和侵袭的增加。总之,WSTF 通过激活 PI3K/AKT 通路促进 GBM 细胞的生长和侵袭。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3158/8611414/fe3b0aa85169/ejh-65-4-3255-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3158/8611414/93a3a9209cd1/ejh-65-4-3255-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3158/8611414/269550248cb0/ejh-65-4-3255-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3158/8611414/b97a84e65c9c/ejh-65-4-3255-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3158/8611414/76395be301ee/ejh-65-4-3255-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3158/8611414/19d431a3c1f5/ejh-65-4-3255-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3158/8611414/fe3b0aa85169/ejh-65-4-3255-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3158/8611414/93a3a9209cd1/ejh-65-4-3255-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3158/8611414/269550248cb0/ejh-65-4-3255-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3158/8611414/b97a84e65c9c/ejh-65-4-3255-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3158/8611414/76395be301ee/ejh-65-4-3255-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3158/8611414/19d431a3c1f5/ejh-65-4-3255-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3158/8611414/fe3b0aa85169/ejh-65-4-3255-g006.jpg

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