Oxygen regulates molecular mechanisms of cancer progression and metastasis

Gupta, Kartik; Madan, Esha; Sayyid, Muzzammil; Arias-Pulido, Hugo; Moreno, Eduardo; Kuppusamy, Periannan; Gogna, Rajan

doi:10.1007/s10555-013-9464-2

Cited by 11 publications

(8 citation statements)

References 283 publications

(351 reference statements)

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“…Mitochondria together with ROS is known to be associated with cell death [63] and several mechanisms implicate these in necroptosis. Zhang [64] reported a lack of phosphorylation of MLKL during myocardial necroptosis in response to ischemia and oxidative stress.…”

Section: Molecular and Cellular Basics Of Necroptosismentioning

confidence: 99%

Necroptosis in cardiovascular disease - a new therapeutic target

Gupta

Phan

Wang

et al. 2018

Journal of Molecular and Cellular Cardiology

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Contrary to the apoptosis-necrosis binary view of cell death, recent experimental evidence demonstrates that several forms of necrosis, represented by necroptosis, are regulated or programmed in nature. Multiple death stimuli known to be associated with cardiovascular disease are capable of causing either apoptosis or necroptosis. Whether a cell dies from apoptosis or necroptosis has distinct consequences on inflammation. It is known that apoptosis, a non-lytic form of death mediated by the caspase family of proteases, does not generally evoke an immune response. Necroptosis, on the other hand, is a lytic form of cell death. Due to the rapid loss of plasma membrane integrity, cells dying from necroptosis release proinflammatory intracellular contents and subsequently cause inflammation. Our review delineates various genetic and biochemical evidence that demonstrates a compelling role of necroptosis in the pathogenesis and/or progression of cardiovascular disease including myocardial infarction, atherosclerosis, and aortic aneurysm. Through recent studies of necroptosis in cardiovascular diseases, we attempt to discuss the role of necroptosis in vascular inflammation as well as the potential of necroptosis inhibitors in future clinical management of cardiovascular events. Inhibiting necroptosis in the vasculature has an overall protective role and necroptosis may represent a new therapeutic target to prevent the development and progression of cardiovascular diseases.

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Section: Molecular and Cellular Basics Of Necroptosismentioning

confidence: 99%

Necroptosis in cardiovascular disease - a new therapeutic target

Gupta

Phan

Wang

et al. 2018

Journal of Molecular and Cellular Cardiology

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“…Depending on the specific cells and tissues undergoing stress, HIFα can mediate adaptive responses to hypoxia that include increased erythropoiesis, increased angiogenesis, and reprogramming of metabolism away from oxidative phosphorylation and towards glycolysis and anaerobic fermentation. In addition to its role in response to acute hypoxic stress, the hypoxia response pathway also helps to maintain stem cell niches and tumor growth and metastasis in cancer ( Amelio and Melino, 2015 ; Gupta et al, 2014 ; Ito and Suda, 2014 ). Whereas the major target of oxygen regulation through EGL-9/PHD proteins is HIFα, several studies have shown that EGL-9/PHD oxygen sensors regulate additional proteins as part of the overall hypoxia response ( Lee et al, 2005 ; Koditz et al, 2007 ; Fu et al, 2007 ; Fu and Taubman, 2010 ; Cummins et al, 2006 ; Park et al, 2012 ; Lee et al, 2015 ).…”

Section: Introductionmentioning

confidence: 99%

The p38 MAP kinase pathway modulates the hypoxia response and glutamate receptor trafficking in aging neurons

Park

Rongo

2016

eLife

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Neurons are sensitive to low oxygen (hypoxia) and employ a conserved pathway to combat its effects. Here, we show that p38 MAP Kinase (MAPK) modulates this hypoxia response pathway in C. elegans. Mutants lacking p38 MAPK components pmk-1 or sek-1 resemble mutants lacking the hypoxia response component and prolyl hydroxylase egl-9, with impaired subcellular localization of Mint orthologue LIN-10, internalization of glutamate receptor GLR-1, and depression of GLR-1-mediated behaviors. Loss of p38 MAPK impairs EGL-9 protein localization in neurons and activates the hypoxia-inducible transcription factor HIF-1, suggesting that p38 MAPK inhibits the hypoxia response pathway through EGL-9. As animals age, p38 MAPK levels decrease, resulting in GLR-1 internalization; this age-dependent downregulation can be prevented through either p38 MAPK overexpression or removal of CDK-5, an antagonizing kinase. Our findings demonstrate that p38 MAPK inhibits the hypoxia response pathway and determines how aging neurons respond to hypoxia through a novel mechanism.DOI: http://dx.doi.org/10.7554/eLife.12010.001

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“…Besides the plasma membrane disruption, MLKL may also target the mitochondrial membrane and induce mitochondrial disruption by opening the mitochondrial permeability transition pore (mPTP) [121,122]. This can result in an excessive production of reactive oxygen species (ROS), further amplifying cell death [123]. It has recently emerged that these MLKL activities do not immediately cause plasma membrane rupture.…”

Section: Mechanisms Underlying Necroptosis: a Broad Overviewmentioning

confidence: 99%

Necroptosis in Immuno-Oncology and Cancer Immunotherapy

Sprooten

Wijngaert

Vanmeerbeek

et al. 2020

Cells

126

112

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Immune-checkpoint blockers (ICBs) have revolutionized oncology and firmly established the subfield of immuno-oncology. Despite this renaissance, a subset of cancer patients remain unresponsive to ICBs due to widespread immuno-resistance. To “break” cancer cell-driven immuno-resistance, researchers have long floated the idea of therapeutically facilitating the immunogenicity of cancer cells by disrupting tumor-associated immuno-tolerance via conventional anticancer therapies. It is well appreciated that anticancer therapies causing immunogenic or inflammatory cell death are best positioned to productively activate anticancer immunity. A large proportion of studies have emphasized the importance of immunogenic apoptosis (i.e., immunogenic cell death or ICD); yet, it has also emerged that necroptosis, a programmed necrotic cell death pathway, can also be immunogenic. Emergence of a proficient immune profile for necroptosis has important implications for cancer because resistance to apoptosis is one of the major hallmarks of tumors. Putative immunogenic or inflammatory characteristics driven by necroptosis can be of great impact in immuno-oncology. However, as is typical for a highly complex and multi-factorial disease like cancer, a clear cause versus consensus relationship on the immunobiology of necroptosis in cancer cells has been tough to establish. In this review, we discuss the various aspects of necroptosis immunobiology with specific focus on immuno-oncology and cancer immunotherapy.

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Oxygen regulates molecular mechanisms of cancer progression and metastasis

Cited by 11 publications

References 283 publications

Necroptosis in cardiovascular disease - a new therapeutic target

Necroptosis in cardiovascular disease - a new therapeutic target

The p38 MAP kinase pathway modulates the hypoxia response and glutamate receptor trafficking in aging neurons

Necroptosis in Immuno-Oncology and Cancer Immunotherapy

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