Role of autophagy in cancer

Mathew, Robin; Karantza‐Wadsworth, Vassiliki; White, Eileen

doi:10.1038/nrc2254

Cited by 1,672 publications

(1,507 citation statements)

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“…Autophagy has been associated with various aspects of innate and adaptive immunity, including interferon and cytokine production (Virgin and Levine, 2009). Moreover, autophagy can be subrogated by cancer cells to avoid the adverse micro-environmental stress (Mathew et al, 2007). Recent data has revealed that sustained activation of ERK and p38 plays critical roles in autophagy at the maturation step (Corcelle et al, 2006).…”

Section: Perspectivesmentioning

confidence: 99%

MAPK signaling in inflammation-associated cancer development

2010

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Mitogen-activated protein (MAP) kinases comprise a family of protein-serine/threonine kinases, which are highly conserved in protein structures from unicellular eukaryotic organisms to multicellular organisms, including mammals. These kinases, including ERKs, JNKs and p38s, are regulated by a phosphorelay cascade, with a prototype of three protein kinases that sequentially phosphorylate one another. MAPKs transduce extracellular signals into a variety of cellular processes, such as cell proliferation, survival, death, and differentiation. Consistent with their essential cellular functions, MAPKs have been shown to play critical roles in embryonic development, adult tissue homeostasis and various pathologies. In this review, we discuss recent findings that reveal the profound impact of these pathways on chronic inflammation and, particularly, inflammation-associated cancer development.

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Section: Perspectivesmentioning

confidence: 99%

MAPK signaling in inflammation-associated cancer development

2010

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“…Secondly an antibody against caspase 3 (which is common to both the extrinsic and intrinsic apoptotic pathways),38 was used to identify cells which may be apoptotic. The third endpoint assessed was autophagy, a self‐digestion process that cells in stressed conditions undergo as part of their normal life cycle,39 but which has been linked to apoptosis 40. Although autophagy has also been implicated in cell survival, an apoptosis‐inducing drug has been previously shown to increase autophagosome numbers in osteosarcoma cells,41 whilst p53 has been shown to activate autophagy so as to increase the efficiency of apoptosis 42.…”

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confidence: 99%

Selective and Potent Proteomimetic Inhibitors of Intracellular Protein–Protein Interactions

et al. 2015

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Inhibition of protein–protein interactions (PPIs) represents a major challenge in chemical biology and drug discovery. α‐Helix mediated PPIs may be amenable to modulation using generic chemotypes, termed “proteomimetics”, which can be assembled in a modular manner to reproduce the vectoral presentation of key side chains found on a helical motif from one partner within the PPI. In this work, it is demonstrated that by using a library of N‐alkylated aromatic oligoamide helix mimetics, potent helix mimetics which reproduce their biophysical binding selectivity in a cellular context can be identified.

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“…Autophagy, or programmed cell survival, shares several common stimuli and signaling pathways with those of apoptosis (Maiuri et al, 2007). Autophagy is a tumorsuppression mechanism, yet it enables tumor-cell survival in settings of enhanced stress (Kondo et al, 2005;Mathew et al, 2007;White and DiPaola, 2009). Moreover, autophagy can degrade active caspase-8 within tumor cells (Hou et al, 2010).…”

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confidence: 99%