Invasion of white matter tracts by glioma stem cells is regulated by a NOTCH1–SOX2 positive-feedback loop

Early invasive growth along specific anatomical structures, especially the white matter tract, is regarded as one of the main causes of poor therapeutic outcome of people with gliomas. We show that some glioma stem cells (GSCs) are preferentially located along white matter tracts, which exhibit a de...

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Published inNature neuroscience Vol. 22; no. 1; pp. 91 - 105
Main Authors Wang, Jun, Xu, Sen-Lin, Duan, Jiang-Jie, Yi, Liang, Guo, Yu-Feng, Shi, Yu, Li, Lin, Yang, Ze-Yu, Liao, Xue-Mei, Cai, Jiao, Zhang, Yan-Qi, Xiao, Hua-Liang, Yin, Li, Wu, Hao, Zhang, Jing-Na, Lv, Sheng-Qing, Yang, Qing-Kai, Yang, Xiao-Jun, Jiang, Tao, Zhang, Xia, Bian, Xiu-Wu, Yu, Shi-Cang
Format Journal Article
LanguageEnglish
Published New York Nature Publishing Group US 01.01.2019
Nature Publishing Group
Subjects
13
13/100
13/109
13/51
13/89
14
14/19
14/28
59
59/36
631/67/1922
631/67/71
631/80/84
692/53/2422
Animal Genetics and Genomics
Attention deficit hyperactivity disorder
Behavioral Sciences
Biological Techniques
Biomedical and Life Sciences
Biomedicine
Brain Neoplasms - diagnostic imaging
Brain Neoplasms - metabolism
Brain Neoplasms - pathology
Cancer invasiveness
Cell Line, Tumor
Cerebral white matter
Control theory
Development and progression
Diffusion Tensor Imaging
DNA methylation
Feedback
Feedback loops
Feedback, Physiological - physiology
Fibers
Genetic aspects
Glioma
Glioma - diagnostic imaging
Glioma - metabolism
Glioma - pathology
Glioma cells
Gliomas
Health aspects
Humans
Jagged-1 Protein - metabolism
Jagged1 protein
Medical imaging equipment
Methylation
Neoplasm Invasiveness - pathology
Neoplastic Stem Cells - metabolism
Neoplastic Stem Cells - pathology
Neurobiology
Neurosciences
Phenotypes
Receptor, Notch1 - metabolism
Sox9 protein
SOXB1 Transcription Factors - metabolism
Stem cells
Substantia alba
Transcription factors
Tropism
White Matter - metabolism
White Matter - pathology
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Abstract Early invasive growth along specific anatomical structures, especially the white matter tract, is regarded as one of the main causes of poor therapeutic outcome of people with gliomas. We show that some glioma stem cells (GSCs) are preferentially located along white matter tracts, which exhibit a demyelinated phenotype, at the invasive frontier of glioma tissues. These GSCs are CD133 + Notch1 + , whereas the nerve fibers express the Notch ligand Jagged1. The Notch-induced transcription factor Sox9 promotes the transcription of SOX2 and the methylation level of the NOTCH1 promoter is attenuated by the upregulation of SOX2 to reinforce NOTCH1 expression in GSCs. This positive-feedback loop in a cohort of glioma subjects is correlated with a poor prognosis. Inhibition of Notch signaling attenuates the white-matter-tract tropism of GSCs. These findings provide evidence indicating that the NOTCH1 - SOX2 positive-feedback loop controls GSC invasion along white matter tracts. CD133 and Notch1 double-positive GSCs were preferentially located along Jagged1-expressing white matter tracts, which exhibited a demyelinated phenotype. The NOTCH1 – SOX9 – SOX2 positive-feedback loop controls GSC invasion along white matter tracts.
AbstractList CD133 and Notch1 double-positive GSCs were preferentially located along Jagged1-expressing white matter tracts, which exhibited a demyelinated phenotype. The NOTCH1–SOX9–SOX2 positive-feedback loop controls GSC invasion along white matter tracts.
Early invasive growth along specific anatomical structures, especially the white matter tract, is regarded as one of the main causes of poor therapeutic outcome of people with gliomas. We show that some glioma stem cells (GSCs) are preferentially located along white matter tracts, which exhibit a demyelinated phenotype, at the invasive frontier of glioma tissues. These GSCs are CD133.sup.+Notch1.sup.+, whereas the nerve fibers express the Notch ligand Jagged1. The Notch-induced transcription factor Sox9 promotes the transcription of SOX2 and the methylation level of the NOTCH1 promoter is attenuated by the upregulation of SOX2 to reinforce NOTCH1 expression in GSCs. This positive-feedback loop in a cohort of glioma subjects is correlated with a poor prognosis. Inhibition of Notch signaling attenuates the white-matter-tract tropism of GSCs. These findings provide evidence indicating that the NOTCH1-SOX2 positive-feedback loop controls GSC invasion along white matter tracts.
Early invasive growth along specific anatomical structures, especially the white matter tract, is regarded as one of the main causes of poor therapeutic outcome of people with gliomas. We show that some glioma stem cells (GSCs) are preferentially located along white matter tracts, which exhibit a demyelinated phenotype, at the invasive frontier of glioma tissues. These GSCs are CD133 + Notch1 + , whereas the nerve fibers express the Notch ligand Jagged1. The Notch-induced transcription factor Sox9 promotes the transcription of SOX2 and the methylation level of the NOTCH1 promoter is attenuated by the upregulation of SOX2 to reinforce NOTCH1 expression in GSCs. This positive-feedback loop in a cohort of glioma subjects is correlated with a poor prognosis. Inhibition of Notch signaling attenuates the white-matter-tract tropism of GSCs. These findings provide evidence indicating that the NOTCH1 - SOX2 positive-feedback loop controls GSC invasion along white matter tracts. CD133 and Notch1 double-positive GSCs were preferentially located along Jagged1-expressing white matter tracts, which exhibited a demyelinated phenotype. The NOTCH1 – SOX9 – SOX2 positive-feedback loop controls GSC invasion along white matter tracts.
Early invasive growth along specific anatomical structures, especially the white matter tract, is regarded as one of the main causes of poor therapeutic outcome of people with gliomas. We show that some glioma stem cells (GSCs) are preferentially located along white matter tracts, which exhibit a demyelinated phenotype, at the invasive frontier of glioma tissues. These GSCs are CD133.sup.+Notch1.sup.+, whereas the nerve fibers express the Notch ligand Jagged1. The Notch-induced transcription factor Sox9 promotes the transcription of SOX2 and the methylation level of the NOTCH1 promoter is attenuated by the upregulation of SOX2 to reinforce NOTCH1 expression in GSCs. This positive-feedback loop in a cohort of glioma subjects is correlated with a poor prognosis. Inhibition of Notch signaling attenuates the white-matter-tract tropism of GSCs. These findings provide evidence indicating that the NOTCH1-SOX2 positive-feedback loop controls GSC invasion along white matter tracts. CD133 and Notch1 double-positive GSCs were preferentially located along Jagged1-expressing white matter tracts, which exhibited a demyelinated phenotype. The NOTCH1-SOX9-SOX2 positive-feedback loop controls GSC invasion along white matter tracts.
Early invasive growth along specific anatomical structures, especially the white matter tract, is regarded as one of the main causes of poor therapeutic outcome of people with gliomas. We show that some glioma stem cells (GSCs) are preferentially located along white matter tracts, which exhibit a demyelinated phenotype, at the invasive frontier of glioma tissues. These GSCs are CD133+Notch1+, whereas the nerve fibers express the Notch ligand Jagged1. The Notch-induced transcription factor Sox9 promotes the transcription of SOX2 and the methylation level of the NOTCH1 promoter is attenuated by the upregulation of SOX2 to reinforce NOTCH1 expression in GSCs. This positive-feedback loop in a cohort of glioma subjects is correlated with a poor prognosis. Inhibition of Notch signaling attenuates the white-matter-tract tropism of GSCs. These findings provide evidence indicating that the NOTCH1-SOX2 positive-feedback loop controls GSC invasion along white matter tracts.Early invasive growth along specific anatomical structures, especially the white matter tract, is regarded as one of the main causes of poor therapeutic outcome of people with gliomas. We show that some glioma stem cells (GSCs) are preferentially located along white matter tracts, which exhibit a demyelinated phenotype, at the invasive frontier of glioma tissues. These GSCs are CD133+Notch1+, whereas the nerve fibers express the Notch ligand Jagged1. The Notch-induced transcription factor Sox9 promotes the transcription of SOX2 and the methylation level of the NOTCH1 promoter is attenuated by the upregulation of SOX2 to reinforce NOTCH1 expression in GSCs. This positive-feedback loop in a cohort of glioma subjects is correlated with a poor prognosis. Inhibition of Notch signaling attenuates the white-matter-tract tropism of GSCs. These findings provide evidence indicating that the NOTCH1-SOX2 positive-feedback loop controls GSC invasion along white matter tracts.
Early invasive growth along specific anatomical structures, especially the white matter tract, is regarded as one of the main causes of poor therapeutic outcome of people with gliomas. We show that some glioma stem cells (GSCs) are preferentially located along white matter tracts, which exhibit a demyelinated phenotype, at the invasive frontier of glioma tissues. These GSCs are CD133 Notch1 , whereas the nerve fibers express the Notch ligand Jagged1. The Notch-induced transcription factor Sox9 promotes the transcription of SOX2 and the methylation level of the NOTCH1 promoter is attenuated by the upregulation of SOX2 to reinforce NOTCH1 expression in GSCs. This positive-feedback loop in a cohort of glioma subjects is correlated with a poor prognosis. Inhibition of Notch signaling attenuates the white-matter-tract tropism of GSCs. These findings provide evidence indicating that the NOTCH1-SOX2 positive-feedback loop controls GSC invasion along white matter tracts.
Audience Academic
Author Zhang, Yan-Qi
Li, Lin
Wu, Hao
Yang, Qing-Kai
Yu, Shi-Cang
Cai, Jiao
Yi, Liang
Wang, Jun
Guo, Yu-Feng
Xiao, Hua-Liang
Zhang, Xia
Yang, Ze-Yu
Duan, Jiang-Jie
Lv, Sheng-Qing
Yin, Li
Xu, Sen-Lin
Liao, Xue-Mei
Bian, Xiu-Wu
Jiang, Tao
Zhang, Jing-Na
Shi, Yu
Yang, Xiao-Jun
Author_xml – sequence: 1
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  surname: Wang
  fullname: Wang, Jun
  organization: Institute of Pathology and Southwest Cancer Center, Key Laboratory of the Ministry of Education, Southwest Hospital, Army Medical University (Third Military Medical University), Department of Stem Cell and Regenerative Medicine, Southwest Hospital, Army Medical University (Third Military Medical University)
– sequence: 2
  givenname: Sen-Lin
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  fullname: Xu, Sen-Lin
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– sequence: 3
  givenname: Jiang-Jie
  surname: Duan
  fullname: Duan, Jiang-Jie
  organization: Institute of Pathology and Southwest Cancer Center, Key Laboratory of the Ministry of Education, Southwest Hospital, Army Medical University (Third Military Medical University), Department of Stem Cell and Regenerative Medicine, Southwest Hospital, Army Medical University (Third Military Medical University)
– sequence: 4
  givenname: Liang
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  organization: Department of Neurosurgery, Daping Hospital, Army Medical University (Third Military Medical University)
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  givenname: Yu-Feng
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  fullname: Guo, Yu-Feng
  organization: Institute of Pathology and Southwest Cancer Center, Key Laboratory of the Ministry of Education, Southwest Hospital, Army Medical University (Third Military Medical University), Department of Stem Cell and Regenerative Medicine, Southwest Hospital, Army Medical University (Third Military Medical University)
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  fullname: Shi, Yu
  organization: Institute of Pathology and Southwest Cancer Center, Key Laboratory of the Ministry of Education, Southwest Hospital, Army Medical University (Third Military Medical University)
– sequence: 7
  givenname: Lin
  surname: Li
  fullname: Li, Lin
  organization: Institute of Pathology and Southwest Cancer Center, Key Laboratory of the Ministry of Education, Southwest Hospital, Army Medical University (Third Military Medical University), Department of Stem Cell and Regenerative Medicine, Southwest Hospital, Army Medical University (Third Military Medical University)
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  givenname: Ze-Yu
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  givenname: Xue-Mei
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  givenname: Jiao
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  organization: Department of Medical Statistics, Military Preventive Medicine Academy, Army Medical University (Third Military Medical University)
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  organization: Department of Pathology, Daping Hospital, Army Medical University (Third Military Medical University)
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  email: yushicang@163.com
  organization: Institute of Pathology and Southwest Cancer Center, Key Laboratory of the Ministry of Education, Southwest Hospital, Army Medical University (Third Military Medical University), Department of Stem Cell and Regenerative Medicine, Southwest Hospital, Army Medical University (Third Military Medical University)
BackLink https://www.ncbi.nlm.nih.gov/pubmed/30559479$$D View this record in MEDLINE/PubMed
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– reference: 30903095 - Nat Neurosci. 2019 May;22(5):840
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Snippet Early invasive growth along specific anatomical structures, especially the white matter tract, is regarded as one of the main causes of poor therapeutic...
CD133 and Notch1 double-positive GSCs were preferentially located along Jagged1-expressing white matter tracts, which exhibited a demyelinated phenotype. The...
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Animal Genetics and Genomics
Attention deficit hyperactivity disorder
Behavioral Sciences
Biological Techniques
Biomedical and Life Sciences
Biomedicine
Brain Neoplasms - diagnostic imaging
Brain Neoplasms - metabolism
Brain Neoplasms - pathology
Cancer invasiveness
Cell Line, Tumor
Cerebral white matter
Control theory
Development and progression
Diffusion Tensor Imaging
DNA methylation
Feedback
Feedback loops
Feedback, Physiological - physiology
Fibers
Genetic aspects
Glioma
Glioma - diagnostic imaging
Glioma - metabolism
Glioma - pathology
Glioma cells
Gliomas
Health aspects
Humans
Jagged-1 Protein - metabolism
Jagged1 protein
Medical imaging equipment
Methylation
Neoplasm Invasiveness - pathology
Neoplastic Stem Cells - metabolism
Neoplastic Stem Cells - pathology
Neurobiology
Neurosciences
Phenotypes
Receptor, Notch1 - metabolism
Sox9 protein
SOXB1 Transcription Factors - metabolism
Stem cells
Substantia alba
Transcription factors
Tropism
White Matter - metabolism
White Matter - pathology
Title Invasion of white matter tracts by glioma stem cells is regulated by a NOTCH1–SOX2 positive-feedback loop
URI https://link.springer.com/article/10.1038/s41593-018-0285-z
https://www.ncbi.nlm.nih.gov/pubmed/30559479
https://www.proquest.com/docview/2157865978
https://www.proquest.com/docview/2158248031
Volume 22
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