Journal
ONCOTARGET
Volume 7, Issue 52, Pages 86117-86133Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.13345
Keywords
newcastle disease virus; endocytosis; clathrin; macropinocytosis; Rab5a
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Funding
- National Natural Science Foundation of China [31402182, 31530074]
- Special Fund for Agro-scientific Research in the Public Interest [201303044, 201303038]
- Key Project of Shanghai Municipal Agricultural Commission [2013-3-7]
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Oncolytic Newcastle disease virus (NDV) reportedly employs direct fusion of the viral envelope with the plasma membrane and caveolae-dependent endocytosis to enter cells. Here, we show that macropinocytosis and clathrin-mediated endocytosis are involved in NDV entry into a galline embryonic fibroblast cell line. Upon specific inhibition of clathrin assembly, GTPase dynamin, Na+/H+ exchangers, Ras-related C3 botulinum toxin substrate 1, p21 activated kinase 1 or protein kinase C, entry of NDV and its propagation were suppressed. NDV entry into cells triggers Rac1-Pak1 signaling and elicits actin rearrangement and plasma membrane ruffling. Moreover, NDV internalization within macropinosomes and trafficking involve Rab5a-positive vesicles. This is the first report demonstrating that NDV utilizes clathrin-mediated endocytosis and macropinocytosis as alternative endocytic pathways to enter cells. These findings shed new light on the molecular mechanisms underlying NDV entry into cells, and provide potential targets for NDV-mediated therapy in cancer.
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