Erratum: Autophagy suppresses tumorigenesis through elimination of p62 (Cell (2009) 137 (1062-1075))

By Robin Mathew, Cristina M. Karp, Brian Beaudoin, N. Vuong, Guanghua Chen, Hsin-Yi Chen, Kevin Bray, Anupama Reddy, G. Bhanot, C. Gélinas and 3 more. 2011

793 citations recorded by the source corpus.

Subfields: Epidemiology

View Paper: https://www.semanticscholar.org/paper/22f238752dd51dd8a84086b664bcfe73ae4aac1f

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In Epidemiology

Citations in the corpus

Recent insights into the function of autophagy in cancer (2016, background): “Autophagy loss in the liver and pancreas causes oxidative stress, chronic tissue damage, and inflammation, all factors that are well known to promote tumor initiation (Mathew et al. 2009).”
Principles and Current Strategies for Targeting Autophagy for Cancer Treatment (2011, methodology): “Indeed, genetic ablation of autophagy sensitizes tumor cells to proteasome inhibitors (35), with combined use of bortezomib and chloroquine increasing tumor cell death in vitro and in vivo (68).”
Autophagy is required to maintain muscle mass. (2009, positive): “It is unclear whether our data of oxidative stress in Atg7 / muscle is mainly caused by accumulation of dysfunctional mitochondria due to a defect in mitophagy, as recently described in autophagy-deficient cells (Tal et al., 2009), or whether it is secondary to p62 aggregates (Mathew et al., 2009).”
Activated Ras requires autophagy to maintain oxidative metabolism and tumorigenesis. (2011, methodology): “Autophagy defects cause accumulation of p62 and ubiquitin (Ub)containing protein aggregates and damaged organelles, particularly mitochondria (Hara et al. 2006; Komatsu et al. 2006, 2007; Mathew et al. 2009).”
Oxidative stress, inflammation, and cancer: how are they linked? (2010, background): “These ROS produced by damaged mitochondria can promote tumor development, probably by perturbing the signal transduction adaptor function of p62-controlling pathways [88].”
Oxidative stress and autophagy: the clash between damage and metabolic needs (2014, background): “damaged mitochondria (mitophagy) and toxic aggregates, autophagy eliminates putative sources of ROS, reduces their levels and, if only indirectly, decreases DNA damage accumulation.(114,121,122) This assumption provides a general explanation of the important role of autophagy in maintaining genomic ”
Persistent activation of Nrf2 through p62 in hepatocellular carcinoma cells (2011, background): “Moreover, dysregulation of NF-B signal in autophagy-incompetent cells was due, at least in part, to accumulation of p62, which subsequently enhanced tumorigenesis (Mathew et al., 2009).”
Hypoxia-induced autophagy: cell death or cell survival? (2010, neutral): “[19 ].”
Eaten alive: a history of macroautophagy (2010, background): “Second, stressed autophagy-defective tumour cells accumulate p62 (also known as sequestosome 1), damaged mitochondria, reactive oxygen species (ROS) and protein aggregates, which might cause DNA damage, oncogene activation and tumorigenesi”
Serine 403 phosphorylation of p62/SQSTM1 regulates selective autophagic clearance of ubiquitinated proteins. (2011, background): “…factor NF-kappa B through binding with atypical PKC (aPKC), RIP1 kinase, or TRAF6 (Chang et al., 2002; Moscat and Diaz-Meco, 2009; Moscat et al., 2006; Sanz et al., 2000; Sanz et al., 1999), in tumorigenesis (Duran et al., 2008; Mathew et al., 2009), and in osteoclastogenesis (Durán et al., 2004).”
Autophagy and aging. (2011, background): “Autophagy can suppress oncogenesis through cell-autonomous effects such as improved quality control of mitochondria, ameliorated genetic instability, and/or the autophagic removal of the potentially oncogenic protein p62/SQTM1 (Mathew et al., 2009).”
The dynamic nature of autophagy in cancer. (2011, background): “…of tumorigenesis through a variety of mechanisms, including deregulation of NF-kB signaling, accumulation of ROS, and increased DNA damage (Mathew et al. 2009). p62 contains a UBA domain, allowing it to bind to ubiquitinated proteins, as well as an LIR (LC3interacting region), conferring…”
The Double-edged Sword of Autophagy Modulation in Cancer (2009, background): “Patients with steatohepatitis are at risk for developing HCC and are a candidate group to test autophagy stimulation for cancer prevention.”
The Role of Autophagy in Cancer: Therapeutic Implications (2011, background): “p62/SQSTM 1 in autophagy-defective cells prevented ROS and theDNAdamage response (17).”
Autophagy: Renovation of Cells and Tissues (2011, background): “This may be due to dysregulation of NF-kB signaling (Mathew et al., 2009) and persistent activation of Nrf2 (DeNicola et al.”