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Anti-angiogenesis effect of trichosanthin and the underlying mechanism
Dongxu He1, Jian Jin, Yongtang Zheng
1National Engineering Laboratory for Cereal Fermentation Technology, Jiangnan University, Wuxi 214122, China.
Abstract:
The growth and metastasis of tumors depend on angiogenesis. Tumor angiogenesis is initiated by the secretion of growth factors from tumor cells; downstream signals are then triggered in pre-existing blood vessels to sprout a new vascular network. Trichosanthin (TCS) is a type I ribosome-inactivating protein that has anti-tumor activity, but the underlying mechanism remains unclear. In this study, we found that a non-toxic dose of TCS decreased the wound-healing and the migration of H5V mouse heart capillary endothelial cells (ECs) induced by human choriocarcinoma (JAR) cells, as well as the JAR-induced angiogenesis of rat third-order mesenteric arteries. TCS was effective on both tumor cells and ECs/arteries. First, TCS decreased vascular endothelial growth factor transcription and secretion by JAR cells. Second, TCS consequently inhibited the tumor cell-induced, extracellular signal-regulated kinase-mediated angiogenic signal in ECs and blood vessels. In conclusion, the ability of TCS to inhibit tumor angiogenesis contributes to its anti-tumor activity.
Insights
Trichosanthin (TCS) inhibits tumor growth by blocking angiogenesis. This anti-tumor protein reduces endothelial cell migration and new blood vessel formation, crucial for tumor development.
Area of Science:
- Oncology
- Vascular Biology
- Biochemistry
Background:
- Tumor growth and metastasis rely on angiogenesis, the formation of new blood vessels.
- Tumor angiogenesis is triggered by growth factors secreted by cancer cells.
- Trichosanthin (TCS), a ribosome-inactivating protein, exhibits anti-tumor properties, but its mechanism is not fully understood.
Purpose of the Study:
- To investigate the anti-angiogenic effects of Trichosanthin (TCS).
- To elucidate the molecular mechanisms by which TCS inhibits tumor angiogenesis.
Main Methods:
- Assessing the effect of TCS on endothelial cell (EC) migration and wound healing.
- Evaluating TCS's impact on angiogenesis in rat mesenteric arteries.
- Measuring vascular endothelial growth factor (VEGF) transcription and secretion.
- Analyzing extracellular signal-regulated kinase (ERK) pathway activation in ECs.
Main Results:
- Non-toxic doses of TCS reduced EC migration and wound healing induced by choriocarcinoma cells.
- TCS inhibited choriocarcinoma-induced angiogenesis in rat mesenteric arteries.
- TCS decreased VEGF transcription and secretion by tumor cells.
- TCS suppressed the ERK-mediated angiogenic signaling pathway in ECs and blood vessels.
Conclusions:
- Trichosanthin (TCS) effectively inhibits tumor angiogenesis.
- TCS acts by reducing VEGF production and downstream signaling in endothelial cells.
- The anti-angiogenic activity of TCS contributes to its overall anti-tumor efficacy.
