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10 results on '"Gutter-Kapon, Lilach"'

6. Significance of host heparanase in promoting tumor growth and metastasis

Author

Zhang, Gan-Lin, primary, Gutter-Kapon, Lilach, additional, Ilan, Neta, additional, Batool, Tahira, additional, Singh, Kailash, additional, Digre, Andreas, additional, Luo, Zhengkang, additional, Sandler, Stellan, additional, Shaked, Yuval, additional, Sanderson, Ralph D., additional, Wang, Xiao-Min, additional, Li, Jin-Ping, additional, and Vlodavsky, Israel, additional

Published
2020
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8. Macrophage-Induced Lymphangiogenesis and Metastasis following Paclitaxel Chemotherapy Is Regulated by VEGFR3

Author

Alishekevitz, Dror, primary, Gingis-Velitski, Svetlana, additional, Kaidar-Person, Orit, additional, Gutter-Kapon, Lilach, additional, Scherer, Sandra D., additional, Raviv, Ziv, additional, Merquiol, Emmanuelle, additional, Ben-Nun, Yael, additional, Miller, Valeria, additional, Rachman-Tzemah, Chen, additional, Timaner, Michael, additional, Mumblat, Yelena, additional, Ilan, Neta, additional, Loven, David, additional, Hershkovitz, Dov, additional, Satchi-Fainaro, Ronit, additional, Blum, Galia, additional, Sleeman, Jonathan P., additional, Vlodavsky, Israel, additional, and Shaked, Yuval, additional

Published
2016
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10. Macrophage-Induced Lymphangiogenesis and Metastasis following Paclitaxel Chemotherapy Is Regulated by VEGFR3

Author

Alishekevitz, Dror, Gingis-Velitski, Svetlana, Kaidar-Person, Orit, Gutter-Kapon, Lilach, Scherer, Sandra D., Raviv, Ziv, Merquiol, Emmanuelle, Ben-Nun, Yael, Miller, Valeria, Rachman-Tzemah, Chen, Timaner, Michael, Mumblat, Yelena, Ilan, Neta, Loven, David, Hershkovitz, Dov, Satchi-Fainaro, Ronit, Blum, Galia, P. Sleeman, Jonathan, Vlodavsky, Israel, and Shaked, Yuval

Subjects
lymphangiogenesis, host response, VEGF-C, chemotherapy, 3. Good health, macrophages, metastatis
Abstract

While chemotherapy strongly restricts or reverses tumor growth, the response of host tissue to therapy can counteract its anti-tumor activity by promoting tumor re-growth and/or metastases, thus limiting therapeutic efficacy. Here, we show that vascular endothelial growth factor receptor 3 (VEGFR3)-expressing macrophages infiltrating chemotherapy-treated tumors play a significant role in metastasis. They do so in part by inducing lymphangiogenesis as a result of cathepsin release, leading to VEGF-C upregulation by heparanase. We found that macrophages from chemotherapy-treated mice are sufficient to trigger lymphatic vessel activity and structure in naive tumors in a VEGFR3-dependent manner. Blocking VEGF-C/VEGFR3 axis inhibits the activity of chemotherapy-educated macrophages, leading to reduced lymphangiogenesis in treated tumors. Overall, our results suggest that disrupting the VEGF-C/VEGFR3 axis not only directly inhibits lymphangiogenesis but also blocks the pro-metastatic activity of macrophages in chemotherapy-treated mice.

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