PMID- 36870690
OWN - NLM
STAT- MEDLINE
DCOM- 20230307
LR  - 20230420
IS  - 1790-6245 (Electronic)
IS  - 1109-6535 (Print)
IS  - 1109-6535 (Linking)
VI  - 20
IP  - 2
DP  - 2023 Mar-Apr
TI  - Myb Repression Mediates Stat5b-knockdown-induced Apoptosis and Inhibits 
      Proliferation of Glioblastoma Stem Cells.
PG  - 195-202
LID - 10.21873/cgp.20374 [doi]
AB  - BACKGROUND/AIM: Glioblastoma is the most common and aggressive malignant brain 
      tumor in adults, and glioblastoma stem cells (GSCs) contribute to treatment 
      resistance and recurrence. Inhibition of Stat5b in GSCs suppresses cell 
      proliferation and induces apoptosis. Herein, we investigated the mechanisms of 
      growth inhibition by Stat5b knockdown (KD) in GSCs. MATERIALS AND METHODS: GSCs 
      were established from a murine glioblastoma model in which shRNA-p53 and EGFR/Ras 
      mutants were induced in vivo using a Sleeping Beauty transposon system. 
      Microarray analyses were performed on Stat5b-KD GSCs to identify genes that are 
      differentially expressed downstream of Stat5b. RT-qPCR and western blot analyses 
      were used to determine Myb levels in GSCs. Myb-overexpressing GSCs were induced 
      by electroporation. Proliferation and apoptosis were evaluated by a trypan blue 
      dye exclusion test and annexin-V staining, respectively. RESULTS: MYB, which is 
      involved in the Wnt pathway, was identified as a novel gene whose expression was 
      down-regulated by Stat5b-KD in GSCs. Both MYB mRNA and protein levels were 
      down-regulated by Stat5b-KD. Overexpression of Myb rescued cell proliferation 
      that was suppressed by Stat5b-KD. Furthermore, Stat5b-KD-induced apoptosis in 
      GSCs was significantly inhibited by Myb overexpression. CONCLUSION: 
      Down-regulation of Myb mediates Stat5b-KD-induced inhibition of proliferation and 
      induction of apoptosis in GSCs. This may represent a promising novel therapeutic 
      strategy against glioblastoma.
CI  - Copyright (c) 2023, International Institute of Anticancer Research (Dr. George J. 
      Delinasios), All rights reserved.
FAU - Moyama, Chiami
AU  - Moyama C
AD  - Department of Clinical Oncology, Kyoto Pharmaceutical University, Kyoto, Japan.
FAU - Fujita, Mitsugu
AU  - Fujita M
AD  - Center for Medical Education and Clinical Training, Faculty of Medicine, Kindai 
      University, Osaka, Japan.
FAU - Okamoto, Hitoshi
AU  - Okamoto H
AD  - Department of Clinical Oncology, Kyoto Pharmaceutical University, Kyoto, Japan.
FAU - Ii, Hiromi
AU  - Ii H
AD  - Department of Clinical Oncology, Kyoto Pharmaceutical University, Kyoto, Japan.
FAU - Nakata, Susumu
AU  - Nakata S
AD  - Department of Clinical Oncology, Kyoto Pharmaceutical University, Kyoto, Japan; 
      snakata@mb.kyoto-phu.ac.jp.
LA  - eng
PT  - Journal Article
PL  - Greece
TA  - Cancer Genomics Proteomics
JT  - Cancer genomics & proteomics
JID - 101188791
RN  - 0 (STAT5B protein, human)
RN  - 0 (STAT5 Transcription Factor)
RN  - 0 (Stat5b protein, mouse)
SB  - IM
MH  - Adult
MH  - Humans
MH  - Animals
MH  - Mice
MH  - *Glioblastoma
MH  - Brain
MH  - Apoptosis
MH  - Cell Proliferation
MH  - Stem Cells
MH  - STAT5 Transcription Factor
PMC - PMC9989674
OTO - NOTNLM
OT  - Glioblastoma stem cells
OT  - Myb
OT  - Stat5b
OT  - Wnt pathway
OT  - apoptosis
COIS- The Authors declare no conflicts of interest pertaining to the present study.
EDAT- 2023/03/05 06:00
MHDA- 2023/03/08 06:00
PMCR- 2023/03/03
CRDT- 2023/03/04 20:42
PHST- 2022/11/24 00:00 [received]
PHST- 2022/12/15 00:00 [revised]
PHST- 2023/01/12 00:00 [accepted]
PHST- 2023/03/04 20:42 [entrez]
PHST- 2023/03/05 06:00 [pubmed]
PHST- 2023/03/08 06:00 [medline]
PHST- 2023/03/03 00:00 [pmc-release]
AID - 20/2/195 [pii]
AID - 10.21873/cgp.20374 [doi]
PST - ppublish
SO  - Cancer Genomics Proteomics. 2023 Mar-Apr;20(2):195-202. doi: 10.21873/cgp.20374.