Published 1982 by U.S. Dept. of Health and Human Services, Public Health Services, National Institutes of Health ; Springfield, Va., National Technical Information Service [distributor in Bethesda, Md .
Written in EnglishRead online
|Statement||Arthur Cederbaum, consulting reivewer.|
|Contributions||Cederbaum, Arthur., International Cancer Research Data Bank.|
|The Physical Object|
|Pagination||ix, 58 p. ;|
|Number of Pages||58|
Download Selected abstracts on mitochondrial respiration in tumor cells and related systems
Get this from a library. Selected abstracts on mitrchondrial respiration in tumor cells and related systems. [Arthur Cederbaum; International Cancer Research Data Bank.; Cancer Information Dissemination and Analysis Center for Virology, Immunology, and Biology.;].
For decades, tumor cells have been considered defective in mitochondrial respiration due to their dominant glycolytic metabolism.
However, a growing body of evidence is now challenging this assumption, and also implying that tumors are metabolically less homogeneous than previously supposed. A small subpopulation of slow-cycling cells endowed with tumorigenic potential and Cited by: Analyzes of macronutrient oxidation, mitochondrial respiration, and expression of genes related to cell metabolism were performed.
The results showed that the trained group had a smaller tumor mass and the mitochondria in the tumors presented lower respiratory rates in the state of maximum electron transport capacity. Warburg’s seminal discovery that cancer cells undergo aerobic glycolysis, which refers to the fermentation of glucose to lactate in the presence of oxygen as opposed to the complete oxidation of glucose to fuel mitochondrial respiration, brought attention to the role of mitochondria Cited by: Cancer is widely considered a genetic disease involving nuclear mutations in oncogenes and tumor suppressor genes.
This view persists despite the numerous inconsistencies associated with the somatic mutation theory. In contrast to the somatic mutation theory, emerging evidence suggests that cancer is a mitochondrial metabolic disease, according to the original theory of Otto by: Tumors and Mitochondrial Respiration: A Neglected Connection Andrea Viale1,2, Denise Corti1,2, and Giulio F.
Draetta1,2 Abstract For decades, tumor cells have been considered defective in mitochondrial respiration due to their dominant glycolytic metabolism. However, a. Mitochondrial defects have long been suspected to play an important role in the development and progression of cancer.
Over 70 years ago, Warburg pioneered the research on mitochondrial respiration alterations in the context of cancer and proposed a mechanism to Selected abstracts on mitochondrial respiration in tumor cells and related systems book how they evolve during the carcinogenic process [1, 2].In his series of landmark publications, he.
When mitochondrial respiration drops below a cell-specific threshold, metabolic reprogramming and plasticity fail to compensate and tumor formation is compromised. In these scenarios, tumorigenesis can be restored by acquisition of respiring mitochondria from surrounding stromal cells.
Multiple molecular features, such as activation of specific oncogenes (e. MYC, BCL2) or a variety of gene expression signatures, have been associated with disease course in diffuse large B-cell lymphoma (DLBCL).
Understanding the relationships between these features and their possible exploitation toward disease classification and therapy remains a major priority in the field. Mitochondrial respiration in plants provides energy for biosynthesis, and its balance with photosynthesis determines the rate of plant biomass accumulation.
We describe recent advances in our understanding of the mitochondrial respiratory machinery of cells, including the presence of a classical oxidative phosphorylation system linked to the cytosol by transporters, discussed alongside.
Shadab Md, in Nanotechnology-Based Targeted Drug Delivery Systems for Lung Cancer, Abstract. Byproducts of cellular respiration, including carbon dioxide, must be removed from cells immediately, through the circulation and finally to the outside of the body via the respiratory system to enable continuation of life and bodily functions.
Mitochondrial respiration occurring in cancer cells might provide a primary source of energy for the low-cycling tumor cells, such as tumor stem cells that are responsible for tumor relapse (Viale. Arsenical inhibition of mitochondrial respiration supported by NA D-linked substrates that use the lipoic acid cofactor for the pyruvate dehydrogenase complex is regarded to be a primary mechanism by which arsenicals produce cell injury/cell death and cancer (Fowler and Woods, ; Fowler et al., ; Chen et al., ; NRC, ).
These stoichiometric data observed in mitochondria from Ehrlich ascites tumor cells thus are in complete agreement with similar data on normal rat liver and rat heart mitochondria and suggest that. The essential hallmarks of cancer are intertwined with an altered cancer cell-intrinsic metabolism, either as a consequence or as a cause.
As an example, the resistance of cancer mitochondria against apoptosis-associated permeabilization and the altered contribution of these organelles to metabolism are closely related.
Similarly, the constitutive activation of signaling cascades that. Charcot–Marie tooth disease is a hereditary polyneuropathy caused by mutations in Mitofusin-2 (MFN2), a GTPase in the outer mitochondrial membrane involved in the regulation of mitochondrial fusion and bioenergetics.
Autosomal-dominant inheritance of a R94Q mutation in MFN2 causes the axonal subtype 2A2A which is characterized by early onset and progressive atrophy of distal muscles caused.
Respiration in intact cells: cellular mitochondrial respiration obtained in the four groups in key parameters of mitochondrial respiration.
Data are mean±s.e.m. The sarcoma group exhibited higher LEAK state and lower MAX/ETS or uncoupled respiration when compared to. In the brain, metastatic breast cancer cells have been shown to be less dependent on glucose, and instead utilize mitochondrial respiration for energy production and antioxidant defense [15, 16].
Moreover, metastatic breast cancer cells have been shown to display neuron-like characteristics in the brain microenvironment [39, 41].
Whether these. Abstract. The fundamental role of mitochondria in energy metabolism and respiration was investigated in stem cells from most of the sources (embryonic, adult, cord blood, and induced pluripotent stem cells (IPSC)).
However, the particular mitochondrial function in cancer stem cells is still under investigation. To further investigate the mechanism of anti-cancer activity, we evaluated the ability of the selected compounds to target mitochondria because inhibition of mitochondrial function by 1,4-NQs can be lethal to a cell.
Complex I consisting of NADH dehydrogenase constitutes one of the major sites of electron entry into the mitochondrial electron. Some abnormalities of mitochondrial function in cancer cells, including metabolic imbalance, enhanced resistance to mitochondrial apoptosis and high incidence of mtDNA mutation, have been revealed by researchers over the past decade.
8 However, the mitochondrial and energy/metabolism‐related phenotypes of CSCs, the stem cell‐like. The tumor microenvironment seems to be another important issue in cancer cell adaptation to different cancer invasion phenotypes.
In summary, the above-mentioned findings suggest that a sufficient supply of ATP by mitochondrial respiration and oxidative phosphorylation is essential for migration and invasion of CRC cells. Metformin is widely used in the treatment of diabetes, and there is interest in ‘repurposing’ the drug for cancer prevention or treatment.
However, the mechanism underlying the metabolic effects of metformin remains poorly understood. We performed respirometry and stable isotope tracer analyses on cells and isolated mitochondria to investigate the impact of metformin on mitochondrial.
Restoration of mitochondrial function is of the utmost importance, since mitochondrial remodeling, or mitochondrial dysbiosis, defined as the process whereby “mitochondria can dissolve their symbiosis with the cell host, and no longer function in harmony with the cell,” is a distal molecular pathway common to all cancer cells (29, 2, p.
Kang BH, Plescia J, Dohi T, Rosa J, Doxsey SJ, Altieri DC. Regulation of tumor cell mitochondrial homeostasis by an organelle-specific Hsp90 chaperone network. Cell. ;(2)– Epub /10/ pmid View Article PubMed/NCBI Google Scholar Mitochondria are exploited in cancer for tumor cell motility, metastatic competence A newly identified pathway for this mechanism also provides a.
Tumorigenic mtDNA mutations affect the respiratory chain complexes and enhance the production of ROS (Brandon et al. ); however, the pathological relevance of mtDNA mutations in cancer cells is controversial (Frezza and Gottlieb ).Nonetheless, a clear-cut correlation between occurrence of pathogenic mtDNA mutations and mitochondrial energetic impairment is a well-demonstrated feature.
Nitric oxide (NO) shows promise either as a cancer therapeutic agent by itself or as a target of cancer therapies. 3 This may be because NO can act as a signaling molecule or as a source of oxidative and nitrosative stress.
4 NO can stimulate mitochondrial biogenesis through PGCrelated coactivator 5 and increase mitochondrial function. 6, 7. Mitochondria Structure and Roles The number of mitochondria per cell is energy/function dependent; i.e., those cells that require and expend the most energy contain the highest number of mitochondria.
Most cells have between a few hundred to o mitochondria; they are concen-trated most heavily in cells of the heart, brain. Abstract. Cancer cells are under intrinsic increased oxidative stress and vulnerable to free radical-induced apoptosis.
Here, we report a strategy to hinder mitochondrial electron transport and increase superoxide radical generation in human leukemia cells as a novel mechanism to enhance apoptosis induced by anticancer agents. This strategy was first tested in a proof-of-principle study.
To directly assess the relative contributions of mitochondrial and plasma membrane redox systems to initial ROS generation after treatment with capsaicin or resiniferatoxin, the authors measured vanilloid-stimulated hydroperoxide generation in ρ 0 clones derived from the SCC cells.
ρ 0 cells exposed to either capsaicin or resiniferatoxin. Human HCT p53 −/− colon cancer cells have previously shown to be sensitive to metformin (Buzzai et al., ).To determine if metformin treatment inhibited cellular oxygen consumption in these cells, we treated HCT p53 −/− cells with increasing concentrations of metformin in media containing the metabolic substrates glucose, pyruvate, and glutamine for 24 hr.
Abstract Mitochondria fuse and divide continuously within cells to form a dynamic network. One of the steps in apoptosis is the fragmentation of mitochondria, and recent evidence indicates that the mitochondrial fission machinery actively participates in the process of programmed cell “Is Cancer Related to Hypertension or to Its.
Thus, we sought to determine whether mitochondrial respiration in circulating cells (peripheral blood mononuclear cells [PBMCs] and platelets) reflects that of skeletal muscle fibers derived from the same subjects.
PBMCs, platelets and skeletal muscle (vastus lateralis) samples were obtained from 32 young ( years) women of varying BMIs. Mitochondria-derived reactive oxygen species (mROS) are required for the survival, proliferation, and metastasis of cancer cells.
The mechanism by which mitochondrial metabolism regulates mROS levels to support cancer cells is not fully understood. To address this, we conducted a metabolism-focused CRISPR-Cas9 genetic screen and uncovered that loss of genes encoding subunits of mitochondrial.
Mitochondria were recently discovered to translocate from one cell to the other. 37 Indeed intercellular mitochondria trafficking was observed in vitro and in vivo, both in physiological and pathophysiological conditions including tissue injury and cancer.
38 In particular, the mitochondria transfer between differentiated and mesenchymal stem. The mitochondrial accumulation of mito-chromanol, a vitamin E analogue conjugated to TPP, induced cell death by inhibiting OXPHOS in breast cancer cells without affecting non-transformed cells.
Background. Placenta-derived mesenchymal stem cells (PD-MSCs) have been highlighted as an alternative cell therapy agent that has become a next-generation stem cell treatment.
Pho. availability of oxygen for use in mitochondrial respiration and synthesis of ATP, forcing cancer cells to up-regulate the glycolytic pathway. In this case, this dependence that confers resistance to cancer cells can be exploited to serve as a biochemical basis to develop therapeutic strategies.
Keywords:Cancer, germline mutation, mitochondrial DNA, mutation pattern. Abstract: It has been suggested that impairment of mitochondrial oxidative phosphorylation (OXPHOS) is a common character in cancer cells, urging attention to variation on mitochondrial DNA (mtDNA) that encodes 13 units of the OXPHOS.
J. Neurochem. ()– Abstract. Parkinson’s disease (PD) is associated with perturbed mitochondrial function.
Studies of cytoplasmic hybrid (cybrid) cell lines containing mitochondria from PD subjects suggest complex I dysfunction in particular is a relatively upstream biochemical defect.Point mutations and copy number changes are the two most common mitochondrial DNA alterations in cancers, and mitochondrial dysfunction induced by chemical depletion of mitochondrial DNA or impairment of mitochondrial respiratory chain in cancer cells promotes cancer progression to a chemoresistance or invasive phenotype.Assessing mitochondrial dysfunction requires definition of the dysfunction to be investigated.
Usually, it is the ability of the mitochondria to make ATP appropriately in response to energy demands. Where other functions are of interest, tailored solutions are required. Dysfunction can be assessed in isolated mitochondria, in cells or in vivo, with different balances between precise.