ArticleInternational journal of molecular sciences2012
Glucose-modulated mitochondria adaptation in tumor cells: a focus on ATP synthase and inhibitor Factor 1.
Article in International journal of molecular sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 50 citations in OpenAlex.
- N-terminal cleavage of cyclophilin D boosts its ability to bind F-ATP synthase.Communications biology · 2024Article
- Multifaceted roles of aerobic glycolysis and oxidative phosphorylation in hepatocellular carcinoma.PeerJ · 2023Review
- Mitochondrial toxicants in Xian-Ling-Gu-Bao induce liver injury by regulating the PI3K/mTOR signaling pathway: an in vitro study.BMC complementary medicine and therapies · 2022Article
- The mesoionic compound MI-D changes energy metabolism and induces apoptosis in T98G glioma cells.Molecular and cellular biochemistry · 2022Article
- Mitochondrial FEMBO reports · 2021Article
- Aglycemic growth enhances carbohydrate metabolism and induces sensitivity to menadione in cultured tumor-derived cells.Cancer & metabolism · 2021Article
- Effects ofBiology · 2018Article
- Reduction of the ATPase inhibitory factor 1 (IFCell death & disease · 2018Article
- Oxidative phosphorylation activation is an important characteristic of DOX resistance in hepatocellular carcinoma cells.Cell communication and signaling : CCS · 2018Article
- Article
- Silver nanoparticles can attenuate nitrative stress.Redox biology · 2017Article
- Dahuang Zhechong Pill Combined with Doxorubicin Induces Cell Death through Regulating Energy Metabolism in Human Hepatocellular Carcinoma Cells.Evidence-based complementary and alternative medicine : eCAM · 2017Article
- Transformation by different oncogenes relies on specific metabolic adaptations.Cell cycle (Georgetown, Tex.) · 2016Article
- ATPase inhibitory factor 1 expression is an independent prognostic factor in non-small cell lung cancer.American journal of cancer research · 2016Article
- Proteomic analysis of Chromobacterium violaceum and its adaptability to stress.BMC microbiology · 2015Article
- Glucose availability determines silver nanoparticles toxicity in HepG2.Journal of nanobiotechnology · 2015Article
- Isothermal microcalorimetry accurately detects bacteria, tumorous microtissues, and parasitic worms in a label-free well-plate assay.Biotechnology journal · 2015Article
- Modulation of mitochondrial bioenergetics in a skeletal muscle cell line model of mitochondrial toxicity.Redox biology · 2014Article
- Metabolic Stress and Disorders Related to Alterations in Mitochondrial Fission or Fusion.Molecular and cellular pharmacology · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Warburg's hypothesis has been challenged by a number of studies showing that oxidative phosphorylation is repressed in some tumors, rather than being inactive per se. Thus, treatments able to shift energy metabolism by activating mitochondrial pathways have been suggested as an intriguing basis for the optimization of antitumor strategies. In this study, HepG2 hepatocarcinoma cells were cultivated with different metabolic substrates under conditions mimicking "positive" (activation/biogenesis) or "negative" (silencing) mitochondrial adaptation. In addition to the expected up-regulation of mitochondrial biogenesis, glucose deprivation caused an increase in phosphorylating respiration and a rise in the expression levels of the ATP synthase β subunit and Inhibitor Factor 1 (IF1). Hyperglycemia, on the other hand, led to a markedly decreased level of the transcriptional coactivator PGC-α suggesting down-regulation of mitochondrial biogenesis, although no change in mitochondrial mass and no impairment of phosphorylating respiration were observed. Moreover, a reduction in mitochondrial networking and in ATP synthase dimer stability was produced. No effect on β-ATP synthase expression was elicited. Notably, hyperglycemia caused an increase in IF1 expression levels, but it did not alter the amount of IF1 associated with ATP synthase. These results point to a new role of IF1 in relation to high glucose utilization by tumor cells, in addition to its well known effect upon mitochondrial ATP synthase regulation.
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