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Related Experiment Video

Updated: Jul 18, 2026

Monitoring Functionality and Morphology of Vasculature Recruited by Factors Secreted by Fast-growing Tumor-generating Cells

Monitoring Functionality and Morphology of Vasculature Recruited by Factors Secreted by Fast-growing Tumor-generating Cells

Published on: November 23, 2014

Pathways targeting tumor lymphangiogenesis.

Christoph Wissmann¹, Michael Detmar

¹Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, Zurich, Switzerland.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research

|December 6, 2006

Summary

Tumor lymphangiogenesis, the growth of lymphatic vessels, promotes cancer spread to lymph nodes. Blocking the VEGF receptor-3 (VEGFR-3) pathway inhibits this process, offering a potential new cancer treatment.

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Published on: January 26, 2024

Area of Science:

Oncology
Molecular Biology
Cancer Research

Background:

Tumor metastasis to sentinel lymph nodes is a critical step in cancer dissemination and a key prognostic indicator.
Tumor-induced lymphangiogenesis (lymphatic vessel formation) correlates with lymph node metastasis in various cancers.
Tumor cells can enhance lymphatic vessel growth post-metastasis, potentially facilitating further spread.

Purpose of the Study:

To investigate the role of tumor lymphangiogenesis in cancer metastasis.
To explore the molecular mechanisms of lymphangiogenesis, particularly the involvement of VEGF-C and VEGF-D via VEGFR-3.
To evaluate the therapeutic potential of targeting the VEGFR-3 pathway for cancer treatment.

Main Methods:

Review of recent studies on tumor lymphangiogenesis and metastasis.
Analysis of the role of Vascular Endothelial Growth Factor-C (VEGF-C) and VEGF-D signaling through VEGF Receptor-3 (VEGFR-3).
Examination of downstream signaling pathways activated by VEGFR-3, including ERK1/2, PI3K/AKT, and JNK1/2.

Main Results:

Tumor lymphangiogenesis is actively induced by tumors and linked to lymph node metastasis.
VEGF-C and VEGF-D are key factors promoting lymphangiogenesis via VEGFR-3 on lymphatic endothelial cells.
VEGFR-3 activation drives lymphatic endothelial cell proliferation, migration, and survival.
Blockade of the VEGFR-3 pathway effectively inhibits experimental tumor lymphangiogenesis and metastasis.

Conclusions:

Tumor lymphangiogenesis is a crucial mechanism in cancer metastasis.
The VEGF-C/VEGF-D/VEGFR-3 pathway is a significant driver of this process.
Targeting the VEGFR-3 pathway presents a promising therapeutic strategy for inhibiting cancer metastasis.