期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 14, 期 1, 页码 88-107出版社
MDPI
DOI: 10.3390/ijms14010088
关键词
VEGF-C; VEGFR-2; VEGFR-3; angiogenesis; lymphangiogenesis; metastasis
资金
- National Science Council grant [NSC 100-2811-B-039-016, NSC 101-2811-B-039-010, NSC 101-2320-B-039-044-MY3, NSC 99-2314-B-039-002-MY3]
- Department of Health, Executive Yuan grant from Taiwan [DOH101-TD-PB-111-NSC015]
- China Medical University [CMU-99-NTU-08, CMU100-TS-06]
- China Medical University Hospital [DMR-101-014]
Vascular endothelial growth factor C (VEGF-C) has been identified as a multifaceted factor participating in the regulation of tumor angiogenesis and lymphangiogenesis. VEGF-C is not only expressed in endothelial cells, but also in tumor cells. VEGF-C signaling is important for progression of various cancer types through both VEGF receptor-2 (VEGFR-2) and VEGF receptor-3 (VEGFR-3). Likewise, both receptors are expressed mainly on endothelial cells, but also expressed in tumor cells. The dimeric VEGF-C undergoes a series of proteolytic cleavage steps that increase the protein binding affinity to VEGFR-3; however, only complete processing, removing both the N- and C-terminal propeptides, yields mature VEGF-C that can bind to VEGFR-2. The processed VEGF-C can bind and activate VEGFR-3 homodimers and VEGFR-2/VEGFR-3 heterodimers to elicit biological responses. High levels of VEGF-C expression and VEGF-C/VEGFRs signaling correlate significantly with poorer prognosis in a variety of malignancies. Therefore, the development of new drugs that selectively target the VEGF-C/VEGFRs axis seems to be an effective means to potentiate anti-tumor therapies in the future.
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