PMID- 21426933
OWN - NLM
STAT- MEDLINE
DCOM- 20110902
LR  - 20211020
IS  - 1873-3913 (Electronic)
IS  - 0898-6568 (Print)
IS  - 0898-6568 (Linking)
VI  - 23
IP  - 8
DP  - 2011 Aug
TI  - Suppression of uPA and uPAR blocks radiation-induced MCP-1 mediated recruitment 
      of endothelial cells in meningioma.
PG  - 1299-310
LID - 10.1016/j.cellsig.2011.03.011 [doi]
AB  - Chemokines play a vital role in recruiting various cell types in the process of 
      tissue repair. Radiation, a major therapeutic modality in cancer treatment, has 
      been described to induce inflammatory response that might lead to the expression 
      of several chemokines. In the present study, we investigated the mechanism of 
      monocyte chemoattractant protein-1 (MCP-1) induction by radiation in meningioma 
      cell lines and the paracrine effect on human microvascular endothelial cells 
      (HMEC). After radiation, meningioma cell lines (IOMM Lee and SF-3061) showed an 
      increased expression of MCP-1. In addition, irradiated meningioma cancer cell 
      conditioned medium (CM) showed an increased ability to attract HMEC and to 
      stimulate MCP-1-induced protein (MCPIP), VEGF and angiogenin expression in HMEC. 
      This chemotactic activity and angiogenic stimulator effect on HMEC were almost 
      abrogated by depleting MCP-1 from the irradiated cancer cell CM. Further, 
      inhibition of either ERK activation/expression or NF-kappaB nuclear translocation 
      hindered radiation-induced MCP-1 expression in both meningioma cell lines. 
      Further, supplementing cancer cells with exogenous ATF-uPA (with and without 
      radiation) activated ERK phosphorylation, nuclear translocation of the NF-kappaB p65 
      sub-unit (Rel-A), and MCP-1 expression. Downregulation of uPA and uPAR, 
      simultaneously by transfecting the cancer cells with bi-cistronic 
      siRNA-expressing plasmid (pU) inhibited radiation-induced ERK activation, nuclear 
      translocation of Rel-A, NF-kappaB DNA binding activity, and MCP-1 expression. In 
      addition, pU-transfected cancer cells (with or without radiation) reduced 
      radiation-induced MCP-1 and blocked the recruitment of other cell types during 
      the inflammatory process induced by radiation both in in vitro and in vivo 
      conditions.
CI  - Copyright (c) 2011 Elsevier Inc. All rights reserved.
FAU - Nalla, Arun Kumar
AU  - Nalla AK
AD  - Department of Cancer Biology and Pharmacology, University of Illinois College of 
      Medicine at Peoria, One Illini Drive, Peoria, IL 61605, USA.
FAU - Gogineni, Venkateswara Rao
AU  - Gogineni VR
FAU - Gupta, Reshu
AU  - Gupta R
FAU - Dinh, Dzung H
AU  - Dinh DH
FAU - Rao, Jasti S
AU  - Rao JS
LA  - eng
GR  - R01 NS061835/NS/NINDS NIH HHS/United States
GR  - R01 NS061835-04/NS/NINDS NIH HHS/United States
GR  - NS061835/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20110321
PL  - England
TA  - Cell Signal
JT  - Cellular signalling
JID - 8904683
RN  - 0 (Chemokine CCL2)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (Receptors, Urokinase Plasminogen Activator)
RN  - 0 (Transcription Factor RelA)
RN  - 0 (Transcription Factors)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
RN  - EC 3.1.- (Ribonucleases)
RN  - EC 3.1.- (ZC3H12A protein, human)
RN  - EC 3.1.27.- (angiogenin)
RN  - EC 3.1.27.5 (Ribonuclease, Pancreatic)
RN  - EC 3.4.21.73 (Urokinase-Type Plasminogen Activator)
SB  - IM
EIN - Cell Signal. 2013 Aug;25(8):1730
MH  - Cell Line, Tumor
MH  - Chemokine CCL2/*metabolism
MH  - Endothelial Cells/*metabolism/radiation effects
MH  - Extracellular Signal-Regulated MAP Kinases/metabolism
MH  - Humans
MH  - Meningeal Neoplasms/*metabolism/radiotherapy
MH  - Meningioma/*metabolism/radiotherapy
MH  - NF-kappa B/metabolism
MH  - Protein Binding
MH  - RNA Interference
MH  - RNA, Small Interfering/metabolism
MH  - Radiation, Ionizing
MH  - Receptors, Urokinase Plasminogen Activator/*antagonists & 
      inhibitors/genetics/metabolism
MH  - Ribonuclease, Pancreatic/metabolism
MH  - Ribonucleases
MH  - Transcription Factor RelA/metabolism
MH  - Transcription Factors/metabolism
MH  - Urokinase-Type Plasminogen Activator/*antagonists & 
      inhibitors/genetics/metabolism
MH  - Vascular Endothelial Growth Factor A/metabolism
PMC - PMC3095686
MID - NIHMS286967
EDAT- 2011/03/24 06:00
MHDA- 2011/09/03 06:00
PMCR- 2012/08/01
CRDT- 2011/03/24 06:00
PHST- 2011/02/01 00:00 [received]
PHST- 2011/03/10 00:00 [revised]
PHST- 2011/03/10 00:00 [accepted]
PHST- 2011/03/24 06:00 [entrez]
PHST- 2011/03/24 06:00 [pubmed]
PHST- 2011/09/03 06:00 [medline]
PHST- 2012/08/01 00:00 [pmc-release]
AID - S0898-6568(11)00086-6 [pii]
AID - 10.1016/j.cellsig.2011.03.011 [doi]
PST - ppublish
SO  - Cell Signal. 2011 Aug;23(8):1299-310. doi: 10.1016/j.cellsig.2011.03.011. Epub 
      2011 Mar 21.