TY - JOUR
T1 - Potential contribution of naïve immune effectors to oral tumor resistance
T2 - Role in synergistic induction of VEGF, IL-6, and IL-8 secretion
AU - Teruel, Antonia
AU - Romero, Marcela
AU - Cacalano, Nicholas A.
AU - Head, Christian
AU - Jewett, Anahid
N1 - Funding Information:
This work was supported by RO1-12880 from NIH-NIDCR.
PY - 2008/3
Y1 - 2008/3
N2 - The aim of this study is to identify the phenotype of resistant oral tumors, and to delineate the contribution of immune effectors to resistance of oral tumors. UCLA-1 oral tumors which were resistant to NK cell mediated cytotoxicity secreted increased amounts of IL-6, IL-1β, GM-CSF, and IL-8 when cultured with or without immune effectors. In addition, the levels of vascular endothelial growth factor (VEGF) secretion in the co-cultures of naïve immune effectors with UCLA-1 rose significantly when compared to tumor cells alone. IL-2 activated NK cells decreased VEGF secretion in all tumor cells. However, NK cells which were induced to undergo cell death with anti-CD16 antibody were not only unable to decrease VEGF secretion, but they also contributed further to the increase in VEGF secretion by oral tumors. Overall, we show in this paper that naïve as well as non-viable immune effectors may contribute to the growth and resistance of oral tumors by triggering the secretion of key tumor cell growth factors.
AB - The aim of this study is to identify the phenotype of resistant oral tumors, and to delineate the contribution of immune effectors to resistance of oral tumors. UCLA-1 oral tumors which were resistant to NK cell mediated cytotoxicity secreted increased amounts of IL-6, IL-1β, GM-CSF, and IL-8 when cultured with or without immune effectors. In addition, the levels of vascular endothelial growth factor (VEGF) secretion in the co-cultures of naïve immune effectors with UCLA-1 rose significantly when compared to tumor cells alone. IL-2 activated NK cells decreased VEGF secretion in all tumor cells. However, NK cells which were induced to undergo cell death with anti-CD16 antibody were not only unable to decrease VEGF secretion, but they also contributed further to the increase in VEGF secretion by oral tumors. Overall, we show in this paper that naïve as well as non-viable immune effectors may contribute to the growth and resistance of oral tumors by triggering the secretion of key tumor cell growth factors.
KW - IFN-γ
KW - IL6
KW - NK cells
KW - Primary oral tumors
KW - UM-SCC-1
KW - VEGF
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U2 - 10.1007/s00262-007-0375-3
DO - 10.1007/s00262-007-0375-3
M3 - Article
C2 - 17703300
AN - SCOPUS:37349072453
SN - 0340-7004
VL - 57
SP - 359
EP - 366
JO - Cancer Immunology, Immunotherapy
JF - Cancer Immunology, Immunotherapy
IS - 3
ER -