We are analyzing https://link.springer.com/article/10.1007/s10495-016-1236-3.

Title:
Unravelling the relationship between macroautophagy and mitochondrial ROS in cancer therapy | Apoptosis
Description:
Macroautophagy (Autophagy), an evolutionarily conserved cellular self-digesting process implicated in various physiological and pathological processes, is activated by different stimuli including oxidative stress. Reactive oxygen species (ROS) are involved in autophagy modulation through multiple signaling pathways and transcription regulators. Accumulating data support both a positive and negative role of ROS-modulated autophagy in cancer. As a tumor suppressive mechanism, autophagy induces autophagic cell death and maintains genome stability. Conversely, autophagy may promote cancer development by limiting metabolic stress and supplying high-energetic nutrients. Mitochondrial ROS (mitoROS), the main source of endogenous ROS, serve as essential signal transducers that mediate autophagy, while autophagy can also regulate mitochondrial ROS generation in turn. Here, we untangle the knot between mitochondrial ROS and autophagy, which may be of great significance to solve the conundrum of the inter-conversion between cytoprotective and cytotoxic roles of autophagy; thus providing new insights for current cancer therapies. Whilst, we focus on anti-tumor agents that target mitoROS-regulated autophagy, in the hope of fueling the exploration of more potential novel anti-cancer drugs in the future.
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28 years and 1 months (reg. 1997-05-29).

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Keywords {🔍}

pubmed, google, scholar, cas, autophagy, cell, central, cancer, cells, mitochondrial, oxygen, reactive, biol, apoptosis, ros, death, species, human, wang, stress, autophagic, oxidative, chen, redox, zhang, therapy, pathways, chem, induces, disease, regulation, article, macroautophagy, huang, signaling, tumor, antioxid, dev, nat, activation, induction, role, signal, anticancer, targeting, metabolism, nature, growth, tumorigenesis, liu,

Topics {✒️}

mitochondria-mediated ros-p38-p53 pathway glycolysis inhibitor 2-deoxy-d-glucose ros–akt–nf-κb pathway mitochondrial electron-transport-chain inhibitors mitochondrial c-raf-dapk complex dap-kinase-mediated phosphorylation short-chain fatty acids month download article/chapter promote oridonin-induced phagocytosis tlr4-mediated skin carcinogenesis important nf-kappab mediator phenethyl isothiocyanate-induced apoptosis hypoxia-induced bnip3 expression supplying high-energetic nutrients ros-mediated autophagy induced γ-tocotrienol induces apoptosis limit caspase-dependent apoptosis cullin-ring ubiquitin ligases reactive oxygen species mir-7-1-3p augmented luteolin hypoxia-tolerant mole rat chemo-resistant melanoma sensitized ros-dependent mitochondrial dysfunction bortezomib/proteasome inhibitor triggers double-edged sword targeting anti-cancer agent lonidamine hypoxia-inducible factor induction nrf2-keap1 antioxidant response extracellular matrix attachment temozolomide-induced cytotoxicity target mitoros-regulated autophagy lung adenomas induced mitochondrial complex ii ros–jnk–autophagy pathway mitochondrial ros production akt signaling pathways privacy choices/manage cookies malignant glioma cells high-androgen responder programmed cell death de witte pa hypoxia-induced autophagy p53-inducible regulator oridonin-induced apoptosis lysosomal degradation pathway ros-mediated mechanism malignant melanoma cells nf-kappab activation multiple signaling pathways promote cancer development

Questions {❓}

Bellot GL, Liu D, Pervaiz S (2013) ROS, autophagy, mitochondria and cancer: Ras, the hidden master?
Green DR, Levine B (2014) To be or not to be?
Malhotra JD, Kaufman RJ (2007) Endoplasmic reticulum stress and oxidative stress: a vicious cycle or a double-edged sword?
Mazure NM, Pouyssegur J (2010) Hypoxia-induced autophagy: cell death or cell survival?
Sabharwal SS, Schumacker PT (2014) Mitochondrial ROS in cancer: initiators, amplifiers or an Achilles’ heel?

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         description:Macroautophagy (Autophagy), an evolutionarily conserved cellular self-digesting process implicated in various physiological and pathological processes, is activated by different stimuli including oxidative stress. Reactive oxygen species (ROS) are involved in autophagy modulation through multiple signaling pathways and transcription regulators. Accumulating data support both a positive and negative role of ROS-modulated autophagy in cancer. As a tumor suppressive mechanism, autophagy induces autophagic cell death and maintains genome stability. Conversely, autophagy may promote cancer development by limiting metabolic stress and supplying high-energetic nutrients. Mitochondrial ROS (mitoROS), the main source of endogenous ROS, serve as essential signal transducers that mediate autophagy, while autophagy can also regulate mitochondrial ROS generation in turn. Here, we untangle the knot between mitochondrial ROS and autophagy, which may be of great significance to solve the conundrum of the inter-conversion between cytoprotective and cytotoxic roles of autophagy; thus providing new insights for current cancer therapies. Whilst, we focus on anti-tumor agents that target mitoROS-regulated autophagy, in the hope of fueling the exploration of more potential novel anti-cancer drugs in the future.
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