PTBP1-mediated alternative splicing regulates the inflammatory secretome and the pro-tumorigenic effects of senescent cells
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Published version
Author(s)
Type
Journal Article
Abstract
Oncogene-induced senescence is a potent tumor-suppressive response. Paradoxically, senescence also induces an inflammatory secretome that promotes carcinogenesis and age-related pathologies. Consequently, the senescence-associated secretory phenotype (SASP) is a potential therapeutic target. Here, we describe an RNAi screen for SASP regulators. We identified 50 druggable targets whose knockdown suppresses the inflammatory secretome and differentially affects other SASP components. Among the screen candidates was PTBP1. PTBP1 regulates the alternative splicing of genes involved in intracellular trafficking, such as EXOC7, to control the SASP. Inhibition of PTBP1 prevents the pro-tumorigenic effects of the SASP and impairs immune surveillance without increasing the risk of tumorigenesis. In conclusion, our study identifies SASP inhibition as a powerful and safe therapy against inflammation-driven cancer.
Date Issued
2018-07-09
Date Acceptance
2018-06-11
Citation
Cancer Cell, 2018, 34 (1), pp.85-102.e9
ISSN
1535-6108
Publisher
Elsevier (Cell Press)
Start Page
85
End Page
102.e9
Journal / Book Title
Cancer Cell
Volume
34
Issue
1
Copyright Statement
© 2018 The Authors. Published by Elsevier Inc. 85This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
Subjects
EXOC7
Oncogene-induced senescence
PTBP1
RNAi screen
SASP
alternative splicing
senescence
1112 Oncology And Carcinogenesis
1109 Neurosciences
Oncology & Carcinogenesis
Publication Status
Published