PMID- 24348834
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20211021
IS  - 1792-1074 (Print)
IS  - 1792-1082 (Electronic)
IS  - 1792-1074 (Linking)
VI  - 7
IP  - 1
DP  - 2014 Jan
TI  - Expression of dedifferentiation markers and multilineage markers in U251 
      glioblastoma cells with silenced EGFR and FGFR genes.
PG  - 131-136
AB  - Epithelial growth factor (EGF) and basic fibroblast growth factor (bFGF), and 
      their receptors, epithelial growth factor receptor (EGFR) and bFGF receptor 
      (bFGFR), are frequently overexpressed in high-grade gliomas. In the present 
      study, the EGF and bFGF levels in U251 glioblastoma cell culture supernatants 
      were determined by ELISA, and enhanced green fluorescent protein (EGFP)-labeled 
      recombinant lentiviral expression vectors with small interfering RNA targeting 
      the EGFR and bFGFR genes were constructed. The mRNA expression levels of EGFR, 
      bFGFR, cluster of differentiation (CD)133, glial fibrillary acidic protein 
      (GFAP), tubulin-beta3 (TUBB3) and myelin basic protein (MBP) were determined using 
      quantitative polymerase chain reactions in U251 cells prior to and following 
      silencing of the EGFR and/or bFGFR genes. Prior to silencing, the U251 cells 
      secreted EGF and bFGF, and expressed EGFR, bFGFR, CD133, GFAP, TUBB3 and MBP 
      mRNA. Subsequent to silencing the EGFR and/or bFGFR gene, CD133 mRNA expression 
      decreased and GFAP and TUBB3 mRNA expression increased. Silencing the EGFR and 
      FGFR genes acted synergistically to downregulate CD133 expression. The 
      downregulation of CD133 mRNA expression and the upregulation of GFAP and TUBB3 
      mRNA expression were not significantly different when blocking the EGFR and FGFR 
      pathways. These results indicate that autocrine or paracrine EGF and/or FGF 
      mechanisms exist in U251 cells. Knocking down the EGFR and/or FGFR genes 
      downregulates CD133 mRNA expression and facilitates glial and neuronal 
      differentiation in U251 cells.
FAU - Xie, Jue
AU  - Xie J
AD  - Department of Blood Transfusion, The First Affiliated Hospital, College of 
      Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China.
FAU - Ma, Yue-Hui
AU  - Ma YH
AD  - Department of Neurosurgery, The First Affiliated Hospital, College of Medicine, 
      Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China.
FAU - Wan, Ming
AU  - Wan M
AD  - Department of Neurosurgery, The First Affiliated Hospital, College of Medicine, 
      Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China.
FAU - Zhan, Ren-Ya
AU  - Zhan RY
AD  - Department of Neurosurgery, The First Affiliated Hospital, College of Medicine, 
      Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China.
FAU - Zhou, Yong-Qing
AU  - Zhou YQ
AD  - Department of Neurosurgery, The First Affiliated Hospital, College of Medicine, 
      Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20131118
PL  - Greece
TA  - Oncol Lett
JT  - Oncology letters
JID - 101531236
PMC - PMC3861577
OTO - NOTNLM
OT  - CD133
OT  - GFAP
OT  - MBP
OT  - TUBB4
OT  - U251 glioblastoma cell
OT  - bFGF
OT  - epidermal growth factor
OT  - small interfering RNA
EDAT- 2013/12/19 06:00
MHDA- 2013/12/19 06:01
PMCR- 2013/11/18
CRDT- 2013/12/19 06:00
PHST- 2013/04/29 00:00 [received]
PHST- 2013/10/31 00:00 [accepted]
PHST- 2013/12/19 06:00 [entrez]
PHST- 2013/12/19 06:00 [pubmed]
PHST- 2013/12/19 06:01 [medline]
PHST- 2013/11/18 00:00 [pmc-release]
AID - ol-07-01-0131 [pii]
AID - 10.3892/ol.2013.1685 [doi]
PST - ppublish
SO  - Oncol Lett. 2014 Jan;7(1):131-136. doi: 10.3892/ol.2013.1685. Epub 2013 Nov 18.