Abstract：
:VEGF/vascular permeability factor (VEGF/VPF or VEGF-A) is a pivotal driver of cancer angiogenesis that is a central therapeutic target in the treatment of malignancy. However, little work has been devoted to investigating functions of VEGF that are independent of its proangiogenic activity. Here, we report that VEGF produced by tumor cells acts in an autocrine manner to promote cell growth through interaction with the VEGF receptor neuropilin-1 (NRP-1). Reducing VEGF expression by tumor cells induced a differentiated phenotype in vitro and inhibited tumor forming capacity in vivo, independent of effects on angiogenesis. Autocrine activation of tumor cell growth was dependent on signaling through NRP-1, and Ras was determined to be a critical effector signaling molecule downstream of NRP-1. Our findings define a novel function for VEGF in dedifferentiation of tumor cells expanding its role in cancer beyond its known proangiogenic function.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Cao Y,E G,Wang E,Pal K,Dutta SK,Bar-Sagi D,Mukhopadhyay Ddoi
10.1158/0008-5472.CAN-11-4058subject
Has Abstractpub_date
2012-08-15 00:00:00pages
3912-8issue
16eissn
0008-5472issn
1538-7445pii
0008-5472.CAN-11-4058journal_volume
72pub_type
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