Aconitase 2 inhibits the proliferation of MCF-7 cells promoting mitochondrial oxidative metabolism and ROS/FoxO1-mediated autophagic response

Background Deregulation of the tricarboxylic acid cycle (TCA) due to mutations in specific enzymes or defective aerobic metabolism is associated with tumour growth. Aconitase 2 (ACO2) participates in the TCA cycle by converting citrate to isocitrate, but no evident demonstrations of its involvement...

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Bibliographic Details
Published in:British journal of cancer 2020-01, Vol.122 (2), p.182-193
Main Authors: Ciccarone, Fabio, Di Leo, Luca, Lazzarino, Giacomo, Maulucci, Giuseppe, Di Giacinto, Flavio, Tavazzi, Barbara, Ciriolo, Maria Rosa
Format: Article
Language:English
Subjects:
631/67/2327
631/80/39
Aconitate Hydratase - antagonists & inhibitors
Aconitate Hydratase - genetics
Adaptation
Autophagy
Autophagy - drug effects
Autophagy - genetics
Bioenergetics
Biomedical and Life Sciences
Biomedicine
Breast cancer
Breast Neoplasms - drug therapy
Breast Neoplasms - genetics
Breast Neoplasms - pathology
Cancer Research
Cell proliferation
Cell Proliferation - drug effects
Citric acid
Drug Resistance
Enzyme Inhibitors - pharmacology
Epidemiology
Evolution
Female
Forkhead Box Protein O1 - genetics
FOXO1 protein
Humans
MCF-7 Cells
Metabolism
Mitochondria
Mitochondria - drug effects
Mitochondria - genetics
Molecular Medicine
Mutation
NADH
Oncology
Oxidative metabolism
Oxidative Stress - drug effects
Phagocytosis
Pyruvic acid
Reactive Oxygen Species - metabolism
Tricarboxylic acid cycle
Tumor cell lines
Tumors
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