Potential contribution of naïve immune effectors to oral tumor resistance: Role in synergistic induction of VEGF, IL-6, and IL-8 secretion

Antonia Teruel, Marcela Romero-Reyes, Nicholas A. Cacalano, Christian Head, Anahid Jewett

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)359-366
Number of pages8
JournalCancer Immunology, Immunotherapy
Volume57
Issue number3
DOIs
StatePublished - Mar 2008

Fingerprint

Interleukin-8
Vascular Endothelial Growth Factor A
Interleukin-6
Neoplasms
Natural Killer Cells
Granulocyte-Macrophage Colony-Stimulating Factor
Coculture Techniques
Interleukin-1
Interleukin-2
Anti-Idiotypic Antibodies
Intercellular Signaling Peptides and Proteins
Cell Death
Phenotype
Growth

Keywords

  • IFN-γ
  • IL6
  • NK cells
  • Primary oral tumors
  • UM-SCC-1
  • VEGF

ASJC Scopus subject areas

  • Cancer Research
  • Immunology
  • Oncology

Cite this

Potential contribution of naïve immune effectors to oral tumor resistance : Role in synergistic induction of VEGF, IL-6, and IL-8 secretion. / Teruel, Antonia; Romero-Reyes, Marcela; Cacalano, Nicholas A.; Head, Christian; Jewett, Anahid.

In: Cancer Immunology, Immunotherapy, Vol. 57, No. 3, 03.2008, p. 359-366.

Research output: Contribution to journalArticle

Teruel, Antonia ; Romero-Reyes, Marcela ; Cacalano, Nicholas A. ; Head, Christian ; Jewett, Anahid. / Potential contribution of naïve immune effectors to oral tumor resistance : Role in synergistic induction of VEGF, IL-6, and IL-8 secretion. In: Cancer Immunology, Immunotherapy. 2008 ; Vol. 57, No. 3. pp. 359-366.
@article{63589c053b1440c88495c7f82f834b01,
title = "Potential contribution of na{\"i}ve immune effectors to oral tumor resistance: Role in synergistic induction of VEGF, IL-6, and IL-8 secretion",
abstract = "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 na{\"i}ve 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 na{\"i}ve 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.",
keywords = "IFN-γ, IL6, NK cells, Primary oral tumors, UM-SCC-1, VEGF",
author = "Antonia Teruel and Marcela Romero-Reyes and Cacalano, {Nicholas A.} and Christian Head and Anahid Jewett",
year = "2008",
month = "3",
doi = "10.1007/s00262-007-0375-3",
language = "English (US)",
volume = "57",
pages = "359--366",
journal = "Cancer Immunology and Immunotherapy",
issn = "0340-7004",
publisher = "Springer Science and Business Media Deutschland GmbH",
number = "3",

}

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-Reyes, Marcela

AU - Cacalano, Nicholas A.

AU - Head, Christian

AU - Jewett, Anahid

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

UR - http://www.scopus.com/inward/record.url?scp=37349072453&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=37349072453&partnerID=8YFLogxK

U2 - 10.1007/s00262-007-0375-3

DO - 10.1007/s00262-007-0375-3

M3 - Article

VL - 57

SP - 359

EP - 366

JO - Cancer Immunology and Immunotherapy

JF - Cancer Immunology and Immunotherapy

SN - 0340-7004

IS - 3

ER -