PMID- 19749789
OWN - NLM
STAT- MEDLINE
DCOM- 20100105
LR  - 20091216
IS  - 1476-5594 (Electronic)
IS  - 0950-9232 (Linking)
VI  - 28
IP  - 49
DP  - 2009 Dec 10
TI  - Pannexin2 as a novel growth regulator in C6 glioma cells.
PG  - 4402-8
LID - 10.1038/onc.2009.283 [doi]
AB  - Connexins (Cxs), the gap junction proteins, have been found to be downregulated 
      in many types of cancers including gliomas. By restoring gap junctional 
      communication in cancer cell models, the neoplastic phenotype can be reversed, 
      suggesting Cxs are tumor suppressors. Pannexin2 (Panx2) is a member of the novel 
      gap junction protein family, Panxs, and it has been proposed as a brain-specific 
      protein. Recently, gene array analysis showed an overall reduction of Panx2 in 
      gliomas, and a direct correlation was observed between Panx2 expression and 
      post-diagnosis survival in patients. In this study, we explored the potential 
      inverse correlation between Panx2 and glioma oncogenicity. A decrease or absence 
      of Panx2 expression in a panel of human glioma cell lines was found, whereas an 
      appreciable amount of Panx2 was detected in both human brain and astrocytes. 
      Stable Panx2 expression revealed a flattened morphology and increased cell-cell 
      contacts in rat C6 glioma cells similar to Panx1. However, in contrast to Panx1 
      and Panx3, Panx2 was predominately detected in the cytoplasm in vesicle-like 
      patterns but not at the plasma membrane. Coexpression of Panx2 and Panx1 did not 
      show colocalization of both Panxs. Strikingly, restoration of Panx2 expression 
      significantly reduced in vitro oncogenicity parameters, including monolayer 
      saturation density and anchorage-independent growth, as well as in vivo tumor 
      growth. This study suggests a role of aberrant Panx2 expression during 
      gliomagenesis, and that Panx2 independently functions as a negative growth 
      regulator without Panx1.
FAU - Lai, C P K
AU  - Lai CP
AD  - Department of Cellular and Physiological Sciences, The Life Sciences Institute, 
      The University of British Columbia, Vancouver, British Columbia, Canada.
FAU - Bechberger, J F
AU  - Bechberger JF
FAU - Naus, C C
AU  - Naus CC
LA  - eng
GR  - Canadian Institutes of Health Research/Canada
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Oncogene
JT  - Oncogene
JID - 8711562
RN  - 0 (Connexins)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 0 (PANX2 protein, human)
SB  - IM
MH  - Animals
MH  - Cell Line, Tumor
MH  - Cell Membrane/metabolism
MH  - *Cell Proliferation
MH  - Connexins/genetics/metabolism/*physiology
MH  - Female
MH  - Gene Expression Regulation, Neoplastic
MH  - Genes, Tumor Suppressor/physiology
MH  - Glioma/genetics/*pathology
MH  - Humans
MH  - Intercellular Signaling Peptides and Proteins/genetics/metabolism/physiology
MH  - Mice
MH  - Mice, Nude
MH  - Mice, SCID
MH  - Mice, Transgenic
MH  - Rats
MH  - Tissue Distribution
MH  - Transplantation, Heterologous
EDAT- 2009/09/15 06:00
MHDA- 2010/01/06 06:00
CRDT- 2009/09/15 06:00
PHST- 2009/09/15 06:00 [entrez]
PHST- 2009/09/15 06:00 [pubmed]
PHST- 2010/01/06 06:00 [medline]
AID - onc2009283 [pii]
AID - 10.1038/onc.2009.283 [doi]
PST - ppublish
SO  - Oncogene. 2009 Dec 10;28(49):4402-8. doi: 10.1038/onc.2009.283.