[HTML][HTML] TBK1 kinase addiction in lung cancer cells is mediated via autophagy of Tax1bp1/Ndp52 and non-canonical NF-κB signalling
AC Newman, CL Scholefield, AJ Kemp, M Newman… - PloS one, 2012 - journals.plos.org
AC Newman, CL Scholefield, AJ Kemp, M Newman, EG McIver, A Kamal, S Wilkinson
PloS one, 2012•journals.plos.orgK-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 …
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 …
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-κB signalling. We propose that this TBK1-dependent mechanism for NF-κB signalling contributes to autophagy addiction in K-Ras driven NSCLC.
PLOS