Regulatory role of c-Met in insulin-like growth factor-I receptor–mediated migration and invasion of human pancreatic carcinoma cells

DOI PDF 被引用文献3件
  • Todd W. Bauer
    1Surgical Oncology and Departments of
  • Ray J. Somcio
    2Cancer Biology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas
  • Fan Fan
    2Cancer Biology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas
  • Wenbiao Liu
    2Cancer Biology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas
  • Marjorie Johnson
    2Cancer Biology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas
  • Donald P. Lesslie
    2Cancer Biology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas
  • Douglas B. Evans
    1Surgical Oncology and Departments of
  • Gary E. Gallick
    2Cancer Biology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas
  • Lee M. Ellis
    1Surgical Oncology and Departments of

抄録

<jats:title>Abstract</jats:title> <jats:p>Pancreatic carcinoma cells overexpress the insulin-like growth factor-I (IGF-I) receptor (IGF-IR) and the hepatocyte growth factor (HGF) receptor, c-Met, which are both known to mediate tumor cell migration and invasion. We hypothesized that IGF-IR and c-Met cooperate to induce migration and invasion of human pancreatic carcinoma cells and that IGF-I-mediated migration and invasion depend on c-Met. Migration and invasion assays were done with the human pancreatic cancer cell line L3.6pl treated with PBS, IGF-I, HGF, or IGF-I plus HGF. To determine if c-Met is necessary for IGF-IR-mediated migration and invasion, c-Met was down-regulated in L3.6pl cells via adenoviral infection with a c-Met ribozyme before IGF-I treatment. IGF-I and HGF increased cell migration and invasion. Furthermore, IGF-I plus HGF had a greater than additive effect on cell migration and invasion compared with either growth factor alone. Down-regulation of c-Met nearly completely inhibited IGF-I-mediated migration and invasion. Our findings suggest that IGF-IR and c-Met cooperate to induce migration and invasion of human pancreatic carcinoma cells. Furthermore, c-Met is required for both HGF- and IGF-I-mediated migration and invasion. Elucidation of the signaling pathways that contribute to tumor progression and metastasis should provide a foundation for the development of targeted therapies for pancreatic carcinoma. [Mol Cancer Ther 2006;5(7):1676–82]</jats:p>

収録刊行物

被引用文献 (3)*注記

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ