Journal
JOURNAL OF CELL SCIENCE
Volume 121, Issue 4, Pages 450-457Publisher
COMPANY BIOLOGISTS LTD
DOI: 10.1242/jcs.022343
Keywords
vFLIP; anoikis; NF-kappa B; endothelial cell
Categories
Funding
- Cancer Research UK Funding Source: Medline
- Wellcome Trust [077161] Funding Source: Medline
Ask authors/readers for more resources
Kaposi's sarcoma-associated herpesvirus (KSHV or HHV-8) infection of endothelial cells is an early event in the aetiology of the endothelial cell tumour Kaposi's sarcoma (KS). We have examined the effect of the KSHV latent protein viral FLICE-like inhibitory protein (vFLIP) on dermal microvascular endothelial cell (MVEC) survival as vFLIP is expressed in the KSHV-infected cells within KS lesions. To do this, we have used a lentiviral vector to express vFLIP in MVECs in the absence of other KSHV proteins. vFLIP activates the classical NF-kappa B pathway in MVECs and causes nuclear translocation of RelA/p65. This NF-kappa B activation prevents detachment-induced apoptosis (anoikis) of MVECs but does not inhibit apoptosis induced by removal of essential survival factors, including vascular endothelial growth factor (VEGF). vFLIP expression inhibits anoikis in part by inducing the secretion of an additional paracrine survival factor(s). The implications of these results for KS development are discussed.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available