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FOXG1 Expression Is Elevated in Glioma and Inhibits Glioma Cell Apoptosis

FOXG1, a member of forkhead family transcriptional factor, is involved in telencephalon development. Recent studies showed FOXG1 was important for a variety of cellular events in cancer cells. In respect to glioma, FOXG1 has been shown to regulate cell proliferation and cell cycles. However, its imp...

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Autores principales: Chen, Jingying, Wu, Xinmin, Xing, Zhenkai, Ma, Chi, Xiong, Wencheng, Zhu, Xiaojuan, He, Xiaoxiao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5868141/
https://www.ncbi.nlm.nih.gov/pubmed/29581755
http://dx.doi.org/10.7150/jca.22282
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author Chen, Jingying
Wu, Xinmin
Xing, Zhenkai
Ma, Chi
Xiong, Wencheng
Zhu, Xiaojuan
He, Xiaoxiao
author_facet Chen, Jingying
Wu, Xinmin
Xing, Zhenkai
Ma, Chi
Xiong, Wencheng
Zhu, Xiaojuan
He, Xiaoxiao
author_sort Chen, Jingying
collection PubMed
description FOXG1, a member of forkhead family transcriptional factor, is involved in telencephalon development. Recent studies showed FOXG1 was important for a variety of cellular events in cancer cells. In respect to glioma, FOXG1 has been shown to regulate cell proliferation and cell cycles. However, its impacts on other cellular events were not well studied. Here, we found FOXG1 had high expression in clinical glioma tissues, and its expression positively correlated with glioma malignancy. Moreover, we found FOXG1 played roles in glioma cell apoptosis. The expressions of caspase family members were significantly altered in response to change of FOXG1 expression, indicating a direct regulation of FOXG1 on caspase family members. These data strongly suggest FOXG1 is negative regulator of glioma cell apoptosis.
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spelling pubmed-58681412018-03-26 FOXG1 Expression Is Elevated in Glioma and Inhibits Glioma Cell Apoptosis Chen, Jingying Wu, Xinmin Xing, Zhenkai Ma, Chi Xiong, Wencheng Zhu, Xiaojuan He, Xiaoxiao J Cancer Short Research Communication FOXG1, a member of forkhead family transcriptional factor, is involved in telencephalon development. Recent studies showed FOXG1 was important for a variety of cellular events in cancer cells. In respect to glioma, FOXG1 has been shown to regulate cell proliferation and cell cycles. However, its impacts on other cellular events were not well studied. Here, we found FOXG1 had high expression in clinical glioma tissues, and its expression positively correlated with glioma malignancy. Moreover, we found FOXG1 played roles in glioma cell apoptosis. The expressions of caspase family members were significantly altered in response to change of FOXG1 expression, indicating a direct regulation of FOXG1 on caspase family members. These data strongly suggest FOXG1 is negative regulator of glioma cell apoptosis. Ivyspring International Publisher 2018-02-11 /pmc/articles/PMC5868141/ /pubmed/29581755 http://dx.doi.org/10.7150/jca.22282 Text en © Ivyspring International Publisher This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) license (https://creativecommons.org/licenses/by-nc/4.0/). See http://ivyspring.com/terms for full terms and conditions.
spellingShingle Short Research Communication
Chen, Jingying
Wu, Xinmin
Xing, Zhenkai
Ma, Chi
Xiong, Wencheng
Zhu, Xiaojuan
He, Xiaoxiao
FOXG1 Expression Is Elevated in Glioma and Inhibits Glioma Cell Apoptosis
title FOXG1 Expression Is Elevated in Glioma and Inhibits Glioma Cell Apoptosis
title_full FOXG1 Expression Is Elevated in Glioma and Inhibits Glioma Cell Apoptosis
title_fullStr FOXG1 Expression Is Elevated in Glioma and Inhibits Glioma Cell Apoptosis
title_full_unstemmed FOXG1 Expression Is Elevated in Glioma and Inhibits Glioma Cell Apoptosis
title_short FOXG1 Expression Is Elevated in Glioma and Inhibits Glioma Cell Apoptosis
title_sort foxg1 expression is elevated in glioma and inhibits glioma cell apoptosis
topic Short Research Communication
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5868141/
https://www.ncbi.nlm.nih.gov/pubmed/29581755
http://dx.doi.org/10.7150/jca.22282
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