PMID- 20969832
OWN - NLM
STAT- MEDLINE
DCOM- 20110321
LR  - 20220408
IS  - 1872-6240 (Electronic)
IS  - 0006-8993 (Linking)
VI  - 1366
DP  - 2010 Dec 17
TI  - Interruption of beta-catenin suppresses the EGFR pathway by blocking multiple 
      oncogenic targets in human glioma cells.
PG  - 27-37
LID - 10.1016/j.brainres.2010.10.032 [doi]
AB  - Malignant gliomas are the most common type of intrinsic central nervous system 
      (CNS) tumors with high mortality and morbidity. beta-catenin is overexpressed in 
      human glioblastoma and knockdown of beta-catenin inhibits glioblastoma cell 
      proliferation and invasive ability, and induces apoptotic cell death. 
      Furthermore, treating the nude mice carrying established subcutaneous LN229 
      gliomas with siRNA targeting beta-catenin intratumorally also delayed the tumor 
      growth. However, the mechanisms of down-regulation of beta-catenin that represses 
      glioblastoma malignancy behavior remain to be elucidated. We utilized text-mining 
      of MEDLINE abstracts with natural language processing to establish the beta-catenin 
      biologic association network, and identified several interactions of this network 
      with the EGFR pathway. In both in vitro and in vivo studies, our results 
      confirmed down-regulation of beta-catenin induced reduced expression of EGFR, STAT3 
      and AKT1 mRNA and protein, besides, the level of phosphorylated Akt also 
      decreased. A similar reduction in expression of CyclinD1, MMP2 and MMP9, 
      downstream genes of the EGFR pathway, was observed. These results suggest that 
      the Wnt/beta-catenin pathway regulates glioma cell proliferation and invasion, in 
      part via the EGFR pathway.
CI  - Copyright (c) 2010 Elsevier B.V. All rights reserved.
FAU - Yue, Xiao
AU  - Yue X
AD  - Laboratory of Neuro-Oncology, Tianjin Neurological Institute, PR China.
FAU - Lan, FengMing
AU  - Lan F
FAU - Yang, WeiDong
AU  - Yang W
FAU - Yang, Yang
AU  - Yang Y
FAU - Han, Lei
AU  - Han L
FAU - Zhang, AnLing
AU  - Zhang A
FAU - Liu, JiLong
AU  - Liu J
FAU - Zeng, HuaZong
AU  - Zeng H
FAU - Jiang, Tao
AU  - Jiang T
FAU - Pu, PeiYu
AU  - Pu P
FAU - Kang, ChunSheng
AU  - Kang C
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20101020
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Carcinogens)
RN  - 0 (RNA, Messenger)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (STAT3 Transcription Factor)
RN  - 0 (STAT3 protein, human)
RN  - 0 (beta Catenin)
RN  - EC 2.7.10.1 (EGFR protein, human)
RN  - EC 2.7.10.1 (ErbB Receptors)
RN  - EC 2.7.11.1 (AKT1 protein, human)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 3.4.24.24 (Matrix Metalloproteinase 2)
SB  - IM
MH  - Animals
MH  - Carcinogens/*metabolism
MH  - Cell Cycle/drug effects/genetics
MH  - Cell Line, Tumor
MH  - Cell Proliferation/drug effects
MH  - Disease Models, Animal
MH  - Down-Regulation/drug effects/genetics
MH  - ErbB Receptors/genetics/*metabolism
MH  - Flow Cytometry/methods
MH  - Glioma/*metabolism/pathology
MH  - Humans
MH  - Matrix Metalloproteinase 2/genetics/metabolism
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Nude
MH  - Proto-Oncogene Proteins c-akt/genetics/metabolism
MH  - RNA, Messenger/metabolism
MH  - RNA, Small Interfering/pharmacology
MH  - STAT3 Transcription Factor/genetics/metabolism
MH  - Signal Transduction/drug effects/*physiology
MH  - beta Catenin/*metabolism
EDAT- 2010/10/26 06:00
MHDA- 2011/03/22 06:00
CRDT- 2010/10/26 06:00
PHST- 2010/07/29 00:00 [received]
PHST- 2010/10/05 00:00 [revised]
PHST- 2010/10/11 00:00 [accepted]
PHST- 2010/10/26 06:00 [entrez]
PHST- 2010/10/26 06:00 [pubmed]
PHST- 2011/03/22 06:00 [medline]
AID - S0006-8993(10)02301-2 [pii]
AID - 10.1016/j.brainres.2010.10.032 [doi]
PST - ppublish
SO  - Brain Res. 2010 Dec 17;1366:27-37. doi: 10.1016/j.brainres.2010.10.032. Epub 2010 
      Oct 20.