AI Article Synopsis
- Controlling lymph node metastasis is crucial in cancer treatment, especially as it significantly affects prognosis in cancers like endometrial cancer.
- Researchers created an animal model using HEC1A endometrial cancer cells, which were injected into mice, leading to lymph node metastasis after 8 weeks.
- By introducing the VEGF-C gene into these cells, they found that higher levels of VEGF-C led to more lymph node metastases, highlighting the importance of VEGF-C in metastasis and its potential for testing new therapies.
Article Abstract
Controlling lymph node metastasis is currently a key issue in cancer therapy. Lymph node metastasis is one of the most important prognostic factors in various types of cancers, including endometrial cancer. Vascular endothelial growth factor-C (VEGF-C) plays a crucial role in lymphangiogenesis, and is implicated to play an important role in lymph node metastasis. To evaluate the role of VEGF-C in lymph node metastasis, we developed an animal model by using an endometrial cancer cell line, HEC1A. This cell line is not invasive by nature and secretes moderate amounts of VEGF-C; intrauterine injection of HEC1A cells into Balb/c nude mice resulted in uterine cancer with lymph node metastasis after 8 weeks. To analyze the contribution of VEGF-C to lymph node metastasis, its corresponding gene was stably introduced into HEC1A cells (HEC1A/VEGF-C), which then produced more than 10 times the amount of VEGF-C. The number of lymph node metastases was significantly higher in HEC1A/VEGF-C cells than in HEC1A cells (3.2 vs 1.1 nodes/animal, respectively). Augmented lymphangiogenesis was observed within tumors when HEC1A/VEGF-C cells were inoculated. These results indicate that VEGF-C plays a critical role in lymph node metastasis, in addition to serving as a platform to test the efficacy of various therapeutic modalities against lymph node metastasis.
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| http://dx.doi.org/10.1111/j.1349-7006.2011.02099.x | DOI Listing |
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