Hypoxia-induced phenotypic transition from highly invasive to less invasive tumors in glioma stem-like cells: Significance of CD44 and osteopontin as therapeutic targets in glioblastoma.

CD44 Glioblastoma Glioma stem cell Hypoxia Osteopontin Tumor progression

Journal

Translational oncology
ISSN: 1936-5233
Titre abrégé: Transl Oncol
Pays: United States
ID NLM: 101472619

Informations de publication

Date de publication:
Aug 2021
Historique:
received: 01 03 2021
revised: 10 05 2021
accepted: 21 05 2021
pubmed: 31 5 2021
medline: 31 5 2021
entrez: 30 5 2021
Statut: ppublish

Résumé

The poor prognosis of glioblastoma multiforme (GBM) is primarily due to highly invasive glioma stem-like cells (GSCs) in tumors. Upon GBM recurrence, GSCs with highly invasive and highly migratory activities must assume a less-motile state and proliferate to regenerate tumor mass. Elucidating the molecular mechanism underlying this transition from a highly invasive phenotype to a less-invasive, proliferative tumor could facilitate the identification of effective molecular targets for treating GBM. Here, we demonstrate that severe hypoxia (1% O

Identifiants

pubmed: 34052625
pii: S1936-5233(21)00129-7
doi: 10.1016/j.tranon.2021.101137
pmc: PMC8175402
pii:
doi:

Types de publication

Journal Article

Langues

eng

Pagination

101137

Informations de copyright

Copyright © 2021. Published by Elsevier Inc.

Auteurs

Masahiro Nishikawa (M)

Department of Neurosurgery, Ehime University Graduate School of Medicine, Toon, Ehime 791-0295, Japan.

Akihiro Inoue (A)

Department of Neurosurgery, Ehime University Graduate School of Medicine, Toon, Ehime 791-0295, Japan. Electronic address: iakihiro@m.ehime-u.ac.jp.

Takanori Ohnishi (T)

Department of Neurosurgery, Washokai Sadamoto Hospital, Matsuyama, Ehime 790-0052, Japan.

Hajime Yano (H)

Department of Molecular and Cellular Physiology, Ehime University Graduate School of Medicine, Toon, Ehime 791-0295, Japan.

Saya Ozaki (S)

Department of Neurosurgery, Ehime University Graduate School of Medicine, Toon, Ehime 791-0295, Japan.

Yonehiro Kanemura (Y)

Department of Biomedical Research and Innovation, Institute for Clinical Research, National Hospital Organization Osaka National Hospital, Osaka 540-0006, Japan; Department of Neurosurgery, National Hospital Organization Osaka National Hospital, Osaka 540-0006, Japan.

Satoshi Suehiro (S)

Department of Neurosurgery, Ehime University Graduate School of Medicine, Toon, Ehime 791-0295, Japan.

Yoshihiro Ohtsuka (Y)

Department of Neurosurgery, Ehime University Graduate School of Medicine, Toon, Ehime 791-0295, Japan.

Shohei Kohno (S)

Department of Neurosurgery, Ehime University Graduate School of Medicine, Toon, Ehime 791-0295, Japan.

Shiro Ohue (S)

Department of Neurosurgery, Ehime Prefectural Central Hospital, Matsuyama, Ehime 790-0024, Japan.

Seiji Shigekawa (S)

Department of Neurosurgery, Ehime University Graduate School of Medicine, Toon, Ehime 791-0295, Japan.

Hideaki Watanabe (H)

Department of Neurosurgery, Ehime University Graduate School of Medicine, Toon, Ehime 791-0295, Japan.

Riko Kitazawa (R)

Division of Diagnostic Pathology, Ehime University Hospital, Toon, Ehime 791-0295, Japan.

Junya Tanaka (J)

Department of Molecular and Cellular Physiology, Ehime University Graduate School of Medicine, Toon, Ehime 791-0295, Japan.

Takeharu Kunieda (T)

Department of Neurosurgery, Ehime University Graduate School of Medicine, Toon, Ehime 791-0295, Japan.

Classifications MeSH