Stressed to death: Mitochondrial stress responses connect respiration and apoptosis in cancer

Mitochondrial energetics and respiration have emerged as important factors in how cancer cells respond to or evade apoptotic signals. The study of the functional connection between these two processes may provide insight into following questions old and new: how might we target respiration or downst...

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Published inMolecular cell Vol. 82; no. 18; pp. 3321 - 3332
Main Authors Winter, Jacob M., Yadav, Tarun, Rutter, Jared
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 15.09.2022
Subjects
Apoptosis
cancer
cancer therapy
CRISPR
death
electron transport chain
Humans
integrated stress response
leukemia
mitochondria
Mitochondria - metabolism
Neoplasms - genetics
Neoplasms - metabolism
oncology
oxidative phosphorylation
Oxidative Stress
Respiration
Signal Transduction
stress
stress response
venetoclax
stress
leukemia
CRISPR
electron transport chain
mitochondria
apoptosis
cancer
respiration
venetoclax
oxidative phosphorylation
oncology
integrated stress response
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Abstract Mitochondrial energetics and respiration have emerged as important factors in how cancer cells respond to or evade apoptotic signals. The study of the functional connection between these two processes may provide insight into following questions old and new: how might we target respiration or downstream signaling pathways to amplify apoptotic stress in the context of cancer therapy? Why are respiration and apoptotic regulation housed in the same organelle? Here, we briefly review mitochondrial respiration and apoptosis and then focus on how the intersection of these two processes is regulated by cytoplasmic signaling pathways such as the integrated stress response. Aerobic respiration and apoptosis are two of the most characteristic activities performed by mitochondria. Here, we review how they are functionally interconnected via stress signaling pathways and describe how these connections might be exploited in the context of cancer therapy.
AbstractList Mitochondrial energetics and respiration have emerged as important factors in how cancer cells respond to or evade apoptotic signals. The study of the functional connection between these two processes may provide insight into following questions old and new: how might we target respiration or downstream signaling pathways to amplify apoptotic stress in the context of cancer therapy? Why are respiration and apoptotic regulation housed in the same organelle? Here, we briefly review mitochondrial respiration and apoptosis and then focus on how the intersection of these two processes is regulated by cytoplasmic signaling pathways such as the integrated stress response.
Mitochondrial energetics and respiration have emerged as important factors in how cancer cells respond to or evade apoptotic signals. The study of the functional connection between these two processes may provide insight into questions old and new, such as: Why are respiration and apoptotic regulation housed in the same organelle? How might we target respiration or downstream signaling pathways to amplify apoptotic stress in the context of cancer therapy? Here we briefly review mitochondrial respiration and apoptosis, and then focus on how the intersection of these two processes is regulated by cytoplasmic signaling pathways such as the integrated stress response. Aerobic respiration and apoptosis are two of the most characteristic activities performed by mitochondria. Here we review how they are functionally interconnected via stress signaling pathways and describe how these connections might be exploited in the context of cancer therapy.
Mitochondrial energetics and respiration have emerged as important factors in how cancer cells respond to or evade apoptotic signals. The study of the functional connection between these two processes may provide insight into following questions old and new: how might we target respiration or downstream signaling pathways to amplify apoptotic stress in the context of cancer therapy? Why are respiration and apoptotic regulation housed in the same organelle? Here, we briefly review mitochondrial respiration and apoptosis and then focus on how the intersection of these two processes is regulated by cytoplasmic signaling pathways such as the integrated stress response.Mitochondrial energetics and respiration have emerged as important factors in how cancer cells respond to or evade apoptotic signals. The study of the functional connection between these two processes may provide insight into following questions old and new: how might we target respiration or downstream signaling pathways to amplify apoptotic stress in the context of cancer therapy? Why are respiration and apoptotic regulation housed in the same organelle? Here, we briefly review mitochondrial respiration and apoptosis and then focus on how the intersection of these two processes is regulated by cytoplasmic signaling pathways such as the integrated stress response.
Mitochondrial energetics and respiration have emerged as important factors in how cancer cells respond to or evade apoptotic signals. The study of the functional connection between these two processes may provide insight into following questions old and new: how might we target respiration or downstream signaling pathways to amplify apoptotic stress in the context of cancer therapy? Why are respiration and apoptotic regulation housed in the same organelle? Here, we briefly review mitochondrial respiration and apoptosis and then focus on how the intersection of these two processes is regulated by cytoplasmic signaling pathways such as the integrated stress response. Aerobic respiration and apoptosis are two of the most characteristic activities performed by mitochondria. Here, we review how they are functionally interconnected via stress signaling pathways and describe how these connections might be exploited in the context of cancer therapy.
Author Yadav, Tarun
Rutter, Jared
Winter, Jacob M.
AuthorAffiliation 2 Department of Biology, Indian Institute of Science Education and Research, Pune
4 Huntsman Cancer Institute, The University of Utah
1 Department of Biochemistry, Spencer Fox Eccles School of Medicine, The University of Utah
3 Howard Hughes Medical Institute, The University of Utah
AuthorAffiliation_xml – name: 1 Department of Biochemistry, Spencer Fox Eccles School of Medicine, The University of Utah
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– name: 4 Huntsman Cancer Institute, The University of Utah
– name: 2 Department of Biology, Indian Institute of Science Education and Research, Pune
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  surname: Winter
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  surname: Rutter
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  email: rutter@biochem.utah.edu
  organization: Department of Biochemistry, Spencer Fox Eccles School of Medicine, The University of Utah, Salt Lake City, UT, USA
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Keywords stress
leukemia
CRISPR
electron transport chain
mitochondria
apoptosis
cancer
respiration
venetoclax
oxidative phosphorylation
oncology
integrated stress response
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Snippet Mitochondrial energetics and respiration have emerged as important factors in how cancer cells respond to or evade apoptotic signals. The study of the...
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SubjectTerms Apoptosis
cancer
cancer therapy
CRISPR
death
electron transport chain
Humans
integrated stress response
leukemia
mitochondria
Mitochondria - metabolism
Neoplasms - genetics
Neoplasms - metabolism
oncology
oxidative phosphorylation
Oxidative Stress
Respiration
Signal Transduction
stress
stress response
venetoclax
Title Stressed to death: Mitochondrial stress responses connect respiration and apoptosis in cancer
URI https://dx.doi.org/10.1016/j.molcel.2022.07.012
https://www.ncbi.nlm.nih.gov/pubmed/35961309
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