vFLIP from KSHV inhibits anoikis of primary endothelial cells.

Journal of Cell Science
Sofia EfklidouMary Collins

Abstract

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-kappaB pathway in MVECs and causes nuclear translocation of RelA/p65. This NF-kappaB 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.

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Citations

Apr 7, 2010·The Journal of Clinical Investigation·Don Ganem
Aug 5, 2009·Cancer Letters·Kwun Wah Wen, Blossom Damania
Jul 20, 2010·Cell Host & Microbe·Samuel H Speck, Don Ganem
Aug 25, 2017·Journal of Cellular Biochemistry·Ehsan KakavandiEbrahim Faghihloo
Oct 1, 2013·Cancers·Therese LiechtensteinDavid Escors
Apr 30, 2017·The Journal of Microbiology·Sangmin Kang, Jinjong Myoung
Aug 8, 2014·Nature Reviews. Cancer·Cassandra L BuchheitZachary T Schafer
Apr 27, 2021·Molecular Therapy. Nucleic Acids·Javid Sadri NahandHamed Mirzaei

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