We are analyzing https://link.springer.com/article/10.1007/s12032-022-01871-0.

Title:
Redox balance and autophagy regulation in cancer progression and their therapeutic perspective | Medical Oncology
Description:
Cellular ROS production participates in various cellular functions but its accumulation decides the cell fate. Malignant cells have higher levels of ROS and active antioxidant machinery, a characteristic hallmark of cancer with an outcome of activation of stress-induced pathways like autophagy. Autophagy is an intracellular catabolic process that produces alternative raw materials to meet the energy demand of cells and is influenced by the cellular redox state thus playing a definite role in cancer cell fate. Since damaged mitochondria are the main source of ROS in the cell, however, cancer cells remove them by upregulating the process of mitophagy which is known to play a decisive role in tumorigenesis and tumor progression. Chemotherapy exploits cell machinery which results in the accumulation of toxic levels of ROS in cells resulting in cell death by activating either of the pathways like apoptosis, necrosis, ferroptosis or autophagy in them. So understanding these redox and autophagy regulations offers a promising method to design and develop new cancer therapies that can be very effective and durable for years. This review will give a summary of the current therapeutic molecules targeting redox regulation and autophagy for the treatment of cancer. Further, it will highlight various challenges in developing anticancer agents due to autophagy and ROS regulation in the cell and insights into the development of future therapies. Graphical Abstract
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28 years and 1 months (reg. 1997-05-29).

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Keywords {🔍}

google, scholar, article, cas, cancer, cell, autophagy, cells, stem, biol, res, mol, breast, wang, zhang, stress, oxidative, regulation, ros, role, tumor, med, redox, reactive, mitochondrial, chen, lee, species, growth, oxygen, sci, targeting, ampk, kinase, protein, metabolism, nat, biochem, signaling, human, rev, resistance, death, survival, therapeutic, liu, clin, kim, progression, apoptosis,

Topics {✒️}

upar/integrin β1/src signaling c-jun nh2-terminal kinase sameer ullah khan ros-p38 mapk pathway-dependent stk11/lkb1-mediated ampk pathway month download article/chapter pi3k/akt/mtor signaling pathway atm-ampk-tsc2–mediated suppression mitogen-activated protein kinases pre-leukemic stem cells amp-activated protein kinase radiation-induced dna damage ultraviolet light-induced generation glutathione s-transferase p1–1 glutathione-s-transferase omega 1 anoikis-resistant cancer cells redox-regulated transcription factors radiation-induced genotoxic stress oxidative stress-induced cancer fayaz malik tumor-initiating cell maintenance nuclear-encoded respiratory genes hypoxia-inducible factor induction axin-ampk-lkb1 complex pro-oxidant redox modifiers parkin-mediated mitochondrial clearance author information authors reactive oxygen species human tomm70 promoter inhibits tumour growth human hepatocellular carcinoma pgc-1α signaling pathways reactive species balance pink1/parkin mitophagy cellular membrane-trafficking system oxidative stress induced hepatocellular carcinoma cells leukemia stem cells fatty acid oxidation stress-induced pathways reactive nitrogen species oxidative dna damage hypoxia-inducible factor 1 crocetin promotes clearance selenium-dependent antioxidant enzymes acute myeloid leukemia accepted manuscript version mesenchymal stem cells radiation-induced bystander nf-κb

Questions {❓}

Mitochondrial ROS in cancer: initiators, amplifiers or an Achilles’ heel?
Mitochondrial oxidative stress drives tumor progression and metastasis: should we use antioxidants as a key component of cancer treatment and prevention?
Mitogen-activated protein kinases and reactive oxygen species: how can ROS activate MAPK pathways?
Superoxide dismutase in gastric adenocarcinoma: is it a clinical biomarker in the development of cancer?
The late stages of autophagy: how does the end begin?
The regulation of autophagy by calcium signals: Do we have a consensus?
What are the hallmarks of cancer?
MTORC1 inhibitors: is temsirolimus in renal cancer telling us how they really work?

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         description:Cellular ROS production participates in various cellular functions but its accumulation decides the cell fate. Malignant cells have higher levels of ROS and active antioxidant machinery, a characteristic hallmark of cancer with an outcome of activation of stress-induced pathways like autophagy. Autophagy is an intracellular catabolic process that produces alternative raw materials to meet the energy demand of cells and is influenced by the cellular redox state thus playing a definite role in cancer cell fate. Since damaged mitochondria are the main source of ROS in the cell, however, cancer cells remove them by upregulating the process of mitophagy which is known to play a decisive role in tumorigenesis and tumor progression. Chemotherapy exploits cell machinery which results in the accumulation of toxic levels of ROS in cells resulting in cell death by activating either of the pathways like apoptosis, necrosis, ferroptosis or autophagy in them. So understanding these redox and autophagy regulations offers a promising method to design and develop new cancer therapies that can be very effective and durable for years. This review will give a summary of the current therapeutic molecules targeting redox regulation and autophagy for the treatment of cancer. Further, it will highlight various challenges in developing anticancer agents due to autophagy and ROS regulation in the cell and insights into the development of future therapies.
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