Dataset related to article "Activation of the VEGFC/VEGFR3 Pathway Induces Tumor Immune Escape in Colorectal Cancer."
Creators
- 1. Humanitas Clinical and Research Center – IRCCS -, via Manzoni 56, 20089 Rozzano (Mi) - Italy
- 2. Department of Internal Medicine, Catholic University of Rome, Rome, Italy.
- 3. School of Medicine and Surgery, University of Milan-Bicocca, Milan, Italy.
- 4. Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, Zurich, Switzerland.
- 5. Humanitas Clinical and Research Center – IRCCS -, via Manzoni 56, 20089 Rozzano (Mi) - Italy AND Humanitas University, Department of Biomedical Sciences, Via Rita Levi Montalcini 4, 20090 Pieve Emanuele – Milan, Italy
- 6. Laboratory of Tumor Inflammation and Angiogenesis, Center for Cancer Biology, Leuven, Belgium.
- 7. Institut National de la Santé et de la Recherche Médicale U954 and Department of Gastroenterology, Nancy University Hospital, Lorraine University, Nancy, France.
Description
Colorectal cancer is a major cause of cancer-related death in Western countries and is associated with increased numbers of lymphatic vessels (LV) and tumor-associated macrophages (TAM). The VEGFC/VEGFR3 pathway is regarded as the principal inducer of lymphangiogenesis and it contributes to metastases; however, no data are available regarding its role during primary colorectal cancer development. We found that both VEGFC and VEGFR3 were upregulated in human nonmetastatic colorectal cancer, with VEGFR3 expressed on both LVs and TAMs. With the use of three different preclinical models of colorectal cancer, we also discovered that the VEGFC/VEGFR3 axis can shape both lymphatic endothelial cells and TAMs to synergistically inhibit antitumor immunity and promote primary colorectal cancer growth. Therefore, VEGFR3-directed therapy could be envisioned for the treatment of nonmetastatic colorectal cancer. SIGNIFICANCE: The prolymphangiogenic factor VEGFC is abundant in colorectal cancer and activates VEGFR3 present on cancer-associated macrophages and lymphatic vessels; activation of VEGFR3 signaling fosters cancer immune escape, resulting in enhanced tumor growth.
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Additional details
Related works
- Is supplement to
- Journal article: 31239267 (PMID)
- Journal article: 10.1158/0008-5472.CAN-18-3657 (DOI)