期刊
PLOS ONE
卷 7, 期 11, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0050672
关键词
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资金
- Cancer Research UK Career Development Fellowship [C20685/A12825]
- Cancer Research UK [12825] Funding Source: researchfish
- Medical Research Council [1137821] Funding Source: researchfish
K-Ras dependent non-small cell lung cancer (NSCLC) cells are 'addicted' to basal autophagy that reprograms cellular metabolism in a lysosomal-sensitive manner. Here we demonstrate that the xenophagy-associated kinase TBK1 drives basal autophagy, consistent with its known requirement in K-Ras-dependent NSCLC proliferation. Furthermore, basal autophagy in this context is characterised by sequestration of the xenophagy cargo receptor Ndp52 and its paralogue Tax1bp1, which we demonstrate here to be a bona fide cargo receptor. Autophagy of these cargo receptors promotes non-canonical NF-kappa B signalling. We propose that this TBK1-dependent mechanism for NF-kappa B signalling contributes to autophagy addiction in K-Ras driven NSCLC. Citation: Newman AC, Scholefield CL, Kemp AJ, Newman M, McIver EG, et al. (2012) TBK1 Kinase Addiction in Lung Cancer Cells Is Mediated via Autophagy of Tax1bp1/Ndp52 and Non-Canonical NF-kappa B Signalling. PLoS ONE 7(11): e50672. doi: 10.1371/journal.pone.0050672
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