IL-1alpha secreted by colon cancer cells enhances angiogenesis: the relationship between IL-1alpha release and tumor cells' potential for liver metastasis

J Surg Oncol. 2009 May 1;99(6):361-7. doi: 10.1002/jso.21245.

Abstract

Background and objectives: Interleukin (IL)-1alpha plays an important role in colon cancer progression and angiogenesis. We here asked whether IL-1alpha derived from cancer cells modulates vascular endothelial cell growth, migration and tubule formation.

Methods: The existence of IL-1alpha mRNA and protein in colon cancer cell lines (WiDr, HT-29, Caco-2, COLO 320) were investigated with RT-PCR and ELISA. Proliferation and invasion were investigated by MTS assay and Matrigel-double chamber assay. To answer our main question, we performed angiogenesis assay used an in vitro model consisting of co-cultivated tumor cells and stromal cells.

Results: IL-1alpha mRNA and protein were detected in highly metastatic colon cancer cells (WiDr and HT-29). Recombinant IL-1alpha significantly enhanced growth and invasiveness of human umbilical vein endothelial cells (HUVEC) (P < 0.01). Moreover, HUVEC growth and migration were significantly enhanced by WiDr compared to control (without co-culture) or Caco-2 (P < 0.05). Exogenous rIL-1alpha significantly enhanced HUVEC tube-like formation in a dose-dependent manner (P < 0.01) in a HUVEC/fibroblast co-cultivation system. Moreover, WiDr significantly enhanced HUVEC tubule formation compared with control or Caco-2 (P < 0.01).

Conclusion: Based on these findings, we conclude that colon cancer cell-derived IL-1alpha up-regulates angiogenesis by modulating stromal cells within the tumor cells' microenvironment.

Publication types

  • Comparative Study

MeSH terms

  • Caco-2 Cells
  • Cell Line, Tumor
  • Cell Proliferation
  • Colonic Neoplasms / blood supply*
  • Colonic Neoplasms / metabolism*
  • Colonic Neoplasms / pathology
  • Enzyme-Linked Immunosorbent Assay
  • Humans
  • Interleukin-1alpha / genetics
  • Interleukin-1alpha / metabolism*
  • Liver Neoplasms / blood supply*
  • Liver Neoplasms / secondary*
  • Neoplasm Invasiveness
  • Neovascularization, Pathologic / metabolism*
  • RNA, Messenger / analysis
  • Reverse Transcriptase Polymerase Chain Reaction

Substances

  • Interleukin-1alpha
  • RNA, Messenger