New aspects of glioblastoma multiforme revealed by similarities between neural and glioblastoma stem cells

Yoichiro Kawamura, Jun Takouda, Koji Yoshimoto, Kinichi Nakashima

研究成果: ジャーナルへの寄稿評論記事

16 引用 (Scopus)

抄録

Neural stem cells (NSCs) undergo self-renewal and generate neurons and glial cells under the influence of specific signals from surrounding environments. Glioblastoma multiforme (GBM) is a highly lethal brain tumor arising from NSCs or glial precursor cells owing to dysregulation of transcriptional and epigenetic networks that control self-renewal and differentiation of NSCs. Highly tumorigenic glioblastoma stem cells (GSCs) constitute a small subpopulation of GBM cells, which share several characteristic similarities with NSCs. GSCs exist atop a stem cell hierarchy and generate heterogeneous populations that participate in tumor propagation, drug resistance, and relapse. During multimodal treatment, GSCs de-differentiate and convert into cells with malignant characteristics, and thus play critical roles in tumor propagation. In contrast, differentiation therapy that induces GBM cells or GSCs to differentiate into a neuronal or glial lineage is expected to inhibit their proliferation. Since stem cell differentiation is specified by the cells’ epigenetic status, understanding their stemness and the epigenomic situation in the ancestor, NSCs, is important and expected to be helpful for developing treatment modalities for GBM. Here, we review the current findings regarding the epigenetic regulatory mechanisms of NSC fate in the developing brain, as well as those of GBM and GSCs. Furthermore, considering the similarities between NSCs and GSCs, we also discuss potential new strategies for GBM treatment.

元の言語英語
ページ(範囲)425-440
ページ数16
ジャーナルCell Biology and Toxicology
34
発行部数6
DOI
出版物ステータス出版済み - 12 15 2018

Fingerprint

Neural Stem Cells
Glioblastoma
Stem cells
Stem Cells
Epigenomics
Neuroglia
Tumors
Brain
Combined Modality Therapy
Gene Regulatory Networks
Drug Resistance
Brain Neoplasms
Cell Differentiation
Neoplasms
Therapeutics
Neurons

All Science Journal Classification (ASJC) codes

  • Toxicology
  • Cell Biology
  • Health, Toxicology and Mutagenesis

これを引用

New aspects of glioblastoma multiforme revealed by similarities between neural and glioblastoma stem cells. / Kawamura, Yoichiro; Takouda, Jun; Yoshimoto, Koji; Nakashima, Kinichi.

:: Cell Biology and Toxicology, 巻 34, 番号 6, 15.12.2018, p. 425-440.

研究成果: ジャーナルへの寄稿評論記事

@article{3029456b143c4b109bbfc22e0ef6e7c2,
title = "New aspects of glioblastoma multiforme revealed by similarities between neural and glioblastoma stem cells",
abstract = "Neural stem cells (NSCs) undergo self-renewal and generate neurons and glial cells under the influence of specific signals from surrounding environments. Glioblastoma multiforme (GBM) is a highly lethal brain tumor arising from NSCs or glial precursor cells owing to dysregulation of transcriptional and epigenetic networks that control self-renewal and differentiation of NSCs. Highly tumorigenic glioblastoma stem cells (GSCs) constitute a small subpopulation of GBM cells, which share several characteristic similarities with NSCs. GSCs exist atop a stem cell hierarchy and generate heterogeneous populations that participate in tumor propagation, drug resistance, and relapse. During multimodal treatment, GSCs de-differentiate and convert into cells with malignant characteristics, and thus play critical roles in tumor propagation. In contrast, differentiation therapy that induces GBM cells or GSCs to differentiate into a neuronal or glial lineage is expected to inhibit their proliferation. Since stem cell differentiation is specified by the cells’ epigenetic status, understanding their stemness and the epigenomic situation in the ancestor, NSCs, is important and expected to be helpful for developing treatment modalities for GBM. Here, we review the current findings regarding the epigenetic regulatory mechanisms of NSC fate in the developing brain, as well as those of GBM and GSCs. Furthermore, considering the similarities between NSCs and GSCs, we also discuss potential new strategies for GBM treatment.",
author = "Yoichiro Kawamura and Jun Takouda and Koji Yoshimoto and Kinichi Nakashima",
year = "2018",
month = "12",
day = "15",
doi = "10.1007/s10565-017-9420-y",
language = "English",
volume = "34",
pages = "425--440",
journal = "Cell Biology and Toxicology",
issn = "0742-2091",
publisher = "Springer Netherlands",
number = "6",

}

TY - JOUR

T1 - New aspects of glioblastoma multiforme revealed by similarities between neural and glioblastoma stem cells

AU - Kawamura, Yoichiro

AU - Takouda, Jun

AU - Yoshimoto, Koji

AU - Nakashima, Kinichi

PY - 2018/12/15

Y1 - 2018/12/15

N2 - Neural stem cells (NSCs) undergo self-renewal and generate neurons and glial cells under the influence of specific signals from surrounding environments. Glioblastoma multiforme (GBM) is a highly lethal brain tumor arising from NSCs or glial precursor cells owing to dysregulation of transcriptional and epigenetic networks that control self-renewal and differentiation of NSCs. Highly tumorigenic glioblastoma stem cells (GSCs) constitute a small subpopulation of GBM cells, which share several characteristic similarities with NSCs. GSCs exist atop a stem cell hierarchy and generate heterogeneous populations that participate in tumor propagation, drug resistance, and relapse. During multimodal treatment, GSCs de-differentiate and convert into cells with malignant characteristics, and thus play critical roles in tumor propagation. In contrast, differentiation therapy that induces GBM cells or GSCs to differentiate into a neuronal or glial lineage is expected to inhibit their proliferation. Since stem cell differentiation is specified by the cells’ epigenetic status, understanding their stemness and the epigenomic situation in the ancestor, NSCs, is important and expected to be helpful for developing treatment modalities for GBM. Here, we review the current findings regarding the epigenetic regulatory mechanisms of NSC fate in the developing brain, as well as those of GBM and GSCs. Furthermore, considering the similarities between NSCs and GSCs, we also discuss potential new strategies for GBM treatment.

AB - Neural stem cells (NSCs) undergo self-renewal and generate neurons and glial cells under the influence of specific signals from surrounding environments. Glioblastoma multiforme (GBM) is a highly lethal brain tumor arising from NSCs or glial precursor cells owing to dysregulation of transcriptional and epigenetic networks that control self-renewal and differentiation of NSCs. Highly tumorigenic glioblastoma stem cells (GSCs) constitute a small subpopulation of GBM cells, which share several characteristic similarities with NSCs. GSCs exist atop a stem cell hierarchy and generate heterogeneous populations that participate in tumor propagation, drug resistance, and relapse. During multimodal treatment, GSCs de-differentiate and convert into cells with malignant characteristics, and thus play critical roles in tumor propagation. In contrast, differentiation therapy that induces GBM cells or GSCs to differentiate into a neuronal or glial lineage is expected to inhibit their proliferation. Since stem cell differentiation is specified by the cells’ epigenetic status, understanding their stemness and the epigenomic situation in the ancestor, NSCs, is important and expected to be helpful for developing treatment modalities for GBM. Here, we review the current findings regarding the epigenetic regulatory mechanisms of NSC fate in the developing brain, as well as those of GBM and GSCs. Furthermore, considering the similarities between NSCs and GSCs, we also discuss potential new strategies for GBM treatment.

UR - http://www.scopus.com/inward/record.url?scp=85041220224&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85041220224&partnerID=8YFLogxK

U2 - 10.1007/s10565-017-9420-y

DO - 10.1007/s10565-017-9420-y

M3 - Review article

C2 - 29383547

AN - SCOPUS:85041220224

VL - 34

SP - 425

EP - 440

JO - Cell Biology and Toxicology

JF - Cell Biology and Toxicology

SN - 0742-2091

IS - 6

ER -