Author/Authors :
Su، نويسنده , , Jen-Liang and Yang، نويسنده , , Pan-Chyr and Shih، نويسنده , , Jin-Yuan and Yang، نويسنده , , Ching-Yao and Wei، نويسنده , , Lin-Hung and Hsieh، نويسنده , , Chang-Yao and Chou، نويسنده , , Chia-Hung and Jeng، نويسنده , , Yung-Ming and Wang، نويسنده , , Ming-Yang and Chang، نويسنده , , King-Jen and Hung، نويسنده , , Mien-Chie and Kuo، نويسنده , , Min-Liang، نويسنده ,
Abstract :
Summary
a VEGF receptor, is activated by its specific ligand, VEGF-C. The resultant signaling pathway promotes angiogenesis and/or lymphangiogenesis. This report provides evidence that the VEGF-C/Flt-4 axis enhances cancer cell mobility and invasiveness and contributes to the promotion of cancer cell metastasis. VEGF-C/Flt-4-mediated invasion and metastasis of cancer cells were found to require upregulation of the neural cell adhesion molecule contactin-1 through activation of the Src-p38 MAPK-C/EBP-dependent pathway. Examination of tumor tissues from various types of cancers revealed high levels of Flt-4 and VEGF-C expression that correlated closely with clinical metastasis and patient survival. The VEGF-C/Flt-4 axis, through upregulation of contactin-1, may regulate the invasive capacity in different types of cancer cells.
