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Cancer Cell death Cell cycle Cytoskeleton Exo/endocytosis Differentiation Division Organelles Signalling Stem cells Trafficking
Cell Biology International (2010) 34, S50 (Printed in Great Britain)
Meeting Abstract
PDCD5 regulates cell autophagy
Yanjun Li12, Lina Chen12, Lanjun Xu12, Dalong Ma12 and Yingyu Chen12
1Laboratory of Medical Immunology, School of Basic Medical Sciences, Peking University Health Science Center, and 2Peking University Center for Human Disease Genomics, Beijing, 100191, China


Programmed Cell Death 5 (PDCD5) is a protein that accelerates apoptosis in different cell types in response to various stimuli, and has been shown to be down-regulated in many cancer tissues. Further investigation reveals that PDCD5 interacts with Tip60 and function as a co-activator to promote apoptosis via the Tip60-p53 signaling pathway. In the present study, we demonstrate a novel feature in the action of PDCD5 on programmed cell death. We found that the clonogenic formation was suppressed in both HEK293 and HeLa cells when PDCD5 expression was stably inhibited by RNA interference. Simultaneously, typical morphological characteristics of autophagy were observed by transmission electron microscopy, including extensive cytoplasmic vacuolization and enclosure of cell organelles by double-membraned structures. Knockdown of PDCD5 expression of enhanced starvation-induced cell autophagy in HeLa. This was indicated by an increase in MDC dot staining and proportion of punctate pattern of LC3 localization, enhancement of Beclin 1 protein expression and decrease of beta-catenin level. Overexpression of PDCD5 partially reversed starvation-induced autophagy. Our preliminary data suggest that PDCD5 may regulate autophagy activation through Wnt signal pathway and function in making trade-offs between apoptosis and autophagy.




Published online 1 August 2010, doi:10.1042/CBI034S050b


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ISSN Print: 1065-6995
ISSN Electronic: 1095-8355
Published by Portland Press Limited on behalf of the International Federation for Cell Biology (IFCB)