TY - JOUR
T1 - Secreted meningeal chemokines, but not VEGFA, modulate the migratory properties of medulloblastoma cells
AU - Davare, Monika A.
AU - Lal, Sangeet
AU - Peckham, Jennifer L.
AU - Prajapati, Suresh I.
AU - Gultekin, Sakir H.
AU - Rubin, Brian P.
AU - Keller, Charles
N1 - Funding Information:
This work was supported in part by a pilot research grant funds from the 2P30CA069533-14 and funds provided to the Knight Cancer Institute at Oregon Health Sciences University by the Schnitzer Investment Corporation. Key equipment was made possible by gifts from the Kyla McCullough Gift Fund .
PY - 2014/7/18
Y1 - 2014/7/18
N2 - Leptomeningeal metastasis is a cause of morbidity and mortality in medulloblastoma, but the understanding of molecular mechanisms driving this process is nascent. In this study, we examined the secretory chemokine profile of medulloblastoma cells (DAOY) and a meningothelial cell line (BMEN1). Conditioned media (CM) of meningothelial cells increased adhesion, spreading and migration of medulloblastoma. VEGFA was identified at elevated levels in the CM from BMEN1 cells (as compared to DAOY CM); however, recombinant VEGFA alone was insufficient to enhance medulloblastoma cell migration. In addition, bevacizumab, the VEGFA scavenging monoclonal antibody, did not block the migratory phenotype induced by the CM. These results reveal that paracrine factors secreted by meningothelial cells can influence migration and adherence of medulloblastoma tumor cells, but VEGFA may not be a specific target for therapeutic intervention in this context.
AB - Leptomeningeal metastasis is a cause of morbidity and mortality in medulloblastoma, but the understanding of molecular mechanisms driving this process is nascent. In this study, we examined the secretory chemokine profile of medulloblastoma cells (DAOY) and a meningothelial cell line (BMEN1). Conditioned media (CM) of meningothelial cells increased adhesion, spreading and migration of medulloblastoma. VEGFA was identified at elevated levels in the CM from BMEN1 cells (as compared to DAOY CM); however, recombinant VEGFA alone was insufficient to enhance medulloblastoma cell migration. In addition, bevacizumab, the VEGFA scavenging monoclonal antibody, did not block the migratory phenotype induced by the CM. These results reveal that paracrine factors secreted by meningothelial cells can influence migration and adherence of medulloblastoma tumor cells, but VEGFA may not be a specific target for therapeutic intervention in this context.
KW - Leptomeningeal metastasis
KW - Medulloblastoma
KW - VEGFA
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U2 - 10.1016/j.bbrc.2014.06.018
DO - 10.1016/j.bbrc.2014.06.018
M3 - Article
C2 - 24928387
AN - SCOPUS:84904763450
SN - 0006-291X
VL - 450
SP - 555
EP - 560
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 1
ER -