Ionizing Radiation Induces Resistant Glioblastoma Stem-Like Cells by Promoting Autophagy via the Wnt/β-Catenin Pathway

Therapeutic resistance in recurrent glioblastoma multiforme (GBM) after concurrent chemoradiotherapy (CCRT) is a challenging issue. Although standard fractionated radiation is essential to treat GBM, it has led to local recurrence along with therapy-resistant cells in the ionizing radiation (IR) fie...

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Veröffentlicht in:Life (Basel, Switzerland) Switzerland), 2021-05, Vol.11 (5), p.451
Hauptverfasser: Tsai, Cheng-Yu, Ko, Huey-Jiun, Huang, Chi-Ying F., Lin, Ching-Yi, Chiou, Shean-Jaw, Su, Yu-Feng, Lieu, Ann-Shung, Loh, Joon-Khim, Kwan, Aij-Lie, Chuang, Tsung-Hsien, Hong, Yi-Ren
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container_issue 5
container_start_page 451
container_title Life (Basel, Switzerland)
container_volume 11
creator Tsai, Cheng-Yu
Ko, Huey-Jiun
Huang, Chi-Ying F.
Lin, Ching-Yi
Chiou, Shean-Jaw
Su, Yu-Feng
Lieu, Ann-Shung
Loh, Joon-Khim
Kwan, Aij-Lie
Chuang, Tsung-Hsien
Hong, Yi-Ren
description Therapeutic resistance in recurrent glioblastoma multiforme (GBM) after concurrent chemoradiotherapy (CCRT) is a challenging issue. Although standard fractionated radiation is essential to treat GBM, it has led to local recurrence along with therapy-resistant cells in the ionizing radiation (IR) field. Lines of evidence showed cancer stem cells (CSCs) play a vital role in therapy resistance in many cancer types, including GBM. However, the molecular mechanism is poorly understood. Here, we proposed that autophagy could be involved in GSC induction for radioresistance. In a clinical setting, patients who received radiation/chemotherapy had higher LC3II expression and showed poor overall survival compared with those with low LC3 II. In a cell model, U87MG and GBM8401 expressed high level of stemness markers CD133, CD44, Nestin, and autophagy marker P62/LC3II after receiving standard fractionated IR. Furthermore, Wnt/β-catenin proved to be a potential pathway and related to P62 by using proteasome inhibitor (MG132). Moreover, pharmacological inhibition of autophagy with BAF and CQ inhibit GSC cell growth by impairing autophagy flux as demonstrated by decrease Nestin, CD133, and SOX-2 levels. In conclusion, we demonstrated that fractionated IR could induce GSCs with the stemness phenotype by P62-mediated autophagy through the Wnt/β-catenin for radioresistance. This study offers a new therapeutic strategy for targeting GBM in the future.
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Although standard fractionated radiation is essential to treat GBM, it has led to local recurrence along with therapy-resistant cells in the ionizing radiation (IR) field. Lines of evidence showed cancer stem cells (CSCs) play a vital role in therapy resistance in many cancer types, including GBM. However, the molecular mechanism is poorly understood. Here, we proposed that autophagy could be involved in GSC induction for radioresistance. In a clinical setting, patients who received radiation/chemotherapy had higher LC3II expression and showed poor overall survival compared with those with low LC3 II. In a cell model, U87MG and GBM8401 expressed high level of stemness markers CD133, CD44, Nestin, and autophagy marker P62/LC3II after receiving standard fractionated IR. Furthermore, Wnt/β-catenin proved to be a potential pathway and related to P62 by using proteasome inhibitor (MG132). Moreover, pharmacological inhibition of autophagy with BAF and CQ inhibit GSC cell growth by impairing autophagy flux as demonstrated by decrease Nestin, CD133, and SOX-2 levels. In conclusion, we demonstrated that fractionated IR could induce GSCs with the stemness phenotype by P62-mediated autophagy through the Wnt/β-catenin for radioresistance. 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subjects Antibodies
Autophagy
Cancer
Cancer therapies
CD44 antigen
Chemoradiotherapy
Chemotherapy
CSC
GBM
Gene expression
Glioblastoma
Glioblastoma multiforme
GSC
Hypoxia
Ionizing radiation
ionizing radiation (IR)
Markers
Medical prognosis
Medical research
Nestin
Phagocytosis
Phenotypes
Proteasome inhibitors
Proteins
Radiation
Radiation standards
Radiation tolerance
Radioresistance
Stem cells
Tumorigenesis
Wnt protein
Wnt/β-Catenin
β-Catenin
title Ionizing Radiation Induces Resistant Glioblastoma Stem-Like Cells by Promoting Autophagy via the Wnt/β-Catenin Pathway
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