Depletion of CXCR2 inhibits tumor growth and angiogenesis in a murine model of lung cancer

J Immunol. 2004 Mar 1;172(5):2853-60. doi: 10.4049/jimmunol.172.5.2853.

Abstract

The Glu-Leu-Arg(+) (ELR(+)) CXC chemokines are potent promoters of angiogenesis and have been demonstrated to induce a significant portion of nonsmall cell lung cancer-derived angiogenic activity and support tumorigenesis. ELR(+) CXC chemokines share a common chemokine receptor, CXCR2. We hypothesized that CXCR2 mediates the proangiogenic effects of ELR(+) CXC chemokines during tumorigenesis. To test this postulate, we used syngeneic murine Lewis lung cancer (LLC; 3LL, H-2(b)) heterotopic and orthotopic tumor model systems in C57BL/6 mice replete (CXCR2(+/+)) and deficient in CXCR2 (CXCR2(-/-)). We first demonstrated a correlation of the expression of endogenous ELR(+) CXC chemokines with tumor growth and metastatic potential of LLC tumors. Next, we found that LLC primary tumors were significantly reduced in growth in CXCR2(-/-) mice. Moreover, we found a marked reduction in the spontaneous metastases of heterotopic tumors to the lungs of CXCR2(-/-) mice. Morphometric analysis of the primary tumors in CXCR2(-/-) mice demonstrated increased necrosis and reduced vascular density. These findings were further confirmed in CXCR2(+/+) mice using specific neutralizing Abs to CXCR2. The results of these studies support the notion that CXCR2 mediates the angiogenic activity of ELR(+) CXC chemokines in a preclinical model of lung cancer.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Carcinoma, Lewis Lung / blood supply
  • Carcinoma, Lewis Lung / pathology
  • Carcinoma, Lewis Lung / prevention & control*
  • Carcinoma, Lewis Lung / secondary
  • Carcinoma, Non-Small-Cell Lung / blood supply
  • Carcinoma, Non-Small-Cell Lung / pathology
  • Carcinoma, Non-Small-Cell Lung / prevention & control*
  • Carcinoma, Non-Small-Cell Lung / secondary
  • Cell Division / genetics
  • Cell Division / immunology
  • Cell Movement / genetics
  • Cell Movement / immunology
  • Chemokine CXCL1
  • Chemokines, CXC / biosynthesis
  • Disease Models, Animal
  • Endothelium, Vascular / immunology
  • Endothelium, Vascular / metabolism
  • Intercellular Signaling Peptides and Proteins / biosynthesis
  • Lung Neoplasms / blood supply
  • Lung Neoplasms / pathology
  • Lung Neoplasms / prevention & control*
  • Lung Neoplasms / secondary
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Molecular Sequence Data
  • Necrosis
  • Neoplasm Transplantation / methods
  • Neovascularization, Pathologic / immunology*
  • Neovascularization, Pathologic / pathology
  • Neovascularization, Pathologic / prevention & control*
  • Receptors, CXCR3
  • Receptors, Chemokine / biosynthesis
  • Receptors, Chemokine / physiology
  • Receptors, Interleukin-8B / biosynthesis
  • Receptors, Interleukin-8B / deficiency*
  • Receptors, Interleukin-8B / genetics*
  • Receptors, Interleukin-8B / physiology
  • Transplantation, Heterotopic / immunology
  • Transplantation, Heterotopic / pathology

Substances

  • Chemokine CXCL1
  • Chemokines, CXC
  • Cxcl1 protein, mouse
  • Cxcr3 protein, mouse
  • Intercellular Signaling Peptides and Proteins
  • Receptors, CXCR3
  • Receptors, Chemokine
  • Receptors, Interleukin-8B