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Promotes Tumor Growth of Lewis Lung Carcinoma by Induction of Angiogenic Factors: In Vivo Analysis of Tumor-Stromal Interaction1
* Department of Respiratory Oncology and Molecular Medicine, Institute of Development, Aging, and Cancer, Tohoku University, Sendai, Japan; and
Department of Molecular Preventive Medicine, School of Medicine, University of Tokyo, Tokyo, Japan
Inflammatory conditions are associated with tumor development.
IL-1
is a multifunctional and proinflammatory cytokine that affects
nearly all types of cells. To investigate the role of IL-1 in tumor
growth in vivo, we transduced the retroviral vector coding human
IL-1 gene into mouse Lewis lung carcinoma
(LLC) cells and subsequently inoculated the transformant (LLC/IL-1)
to syngeneic C57BL/6 mice. Tumors derived from LLC/IL-1 grew faster
(240%, day 18, vs null-vector control LLC/neo; p
< 0.01) and showed more abundant vasculature (250%, vs LLC/neo;
p < 0.05), whereas LLC/IL-1 cells, LLC/neo
cells, and wild-type LLC cells did not show any significant difference
in the growth rate in vitro. As compared with LLC/neo cells,
LLC/IL-1 cells secreted 2-fold the amount of vascular endothelial
growth factor and >10-fold the amount of macrophage-inflammatory
protein-2 (CXCL2), one of whose main functions is angiogenesis.
Although LLC/IL-1 itself did not secrete hepatocyte growth factor
(HGF), the tumor derived from LLC/IL-1 cells also contained a
>4-fold higher concentration of HGF, another angiogenic factor.
In situ hybridization of HGF mRNA in LLC/IL-1 tumor sections
demonstrated that stromal fibroblasts and infiltrating cells
overexpressed HGF mRNA. Moreover, when cultured in the presence of HGF
in vitro, LLC/IL-1 cells secreted even larger amounts of vascular
endothelial growth factor and macrophage-inflammatory protein-2. The
antiangiogenic agent TNP-470 and anti-CXCR2 Ab inhibited the tumor
growth of LLC/IL-1 cells in vivo. These results indicated that
secreting IL-1 into the tumor milieu induces several angiogenic
factors from tumor and stromal cells and thus promotes tumor growth
through hyperneovascularization.
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