ArticleIranian journal of basic medical sciences2015
Investigation on metabolism of cisplatin resistant ovarian cancer using a genome scale metabolic model and microarray data.
Article in Iranian journal of basic medical sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Transcriptome-driven constraint-based modelling reveals metabolic targets for ovarian cancer.Cancer & metabolism · 2026Article
- Constraint-based modelling predicts metabolic signatures of low and high-grade serous ovarian cancer.NPJ systems biology and applications · 2024Article
- Article
- The role of PYCR1 in inhibiting 5-fluorouracil-induced ferroptosis and apoptosis through SLC25A10 in colorectal cancer.Human cell · 2022Article
- MIR600HG sponges miR-125a-5p to regulate glycometabolism and cisplatin resistance of oral squamous cell carcinoma cells via mediating RNF44.Cell death discovery · 2022Article
- Article
- Genome Scale Modeling to Study the Metabolic Competition between Cells in the Tumor Microenvironment.Cancers · 2021Review
- Cisplatin and phenanthriplatin modulate long-noncoding RNA expression in A549 and IMR90 cells revealing regulation of microRNAs, Wnt/β-catenin and TGF-β signaling.Scientific reports · 2021Article
- Analyzing Metabolic States of Adipogenic and Osteogenic Differentiation in Human Mesenchymal Stem Cells via Genome Scale Metabolic Model Reconstruction.Frontiers in cell and developmental biology · 2021Article
- Applications of Multi-omics Approaches for Exploring the Molecular Mechanism of Ovarian Carcinogenesis.Frontiers in oncology · 2021Review
- Article
- Proliferation inhibition of cisplatin-resistant ovarian cancer cells using drugs screened by integrating a metabolic model and transcriptomic data.Cell proliferation · 2017Article
- pETM: a penalized Exponential Tilt Model for analysis of correlated high-dimensional DNA methylation data.Bioinformatics (Oxford, England) · 2017Article
- 14-3-3σ confers cisplatin resistance in esophageal squamous cell carcinoma cells via regulating DNA repair molecules.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Understanding the Causes and Implications of Endothelial Metabolic Variation in Cardiovascular Disease through Genome-Scale Metabolic Modeling.Frontiers in cardiovascular medicine · 2016Review
- MiR-122 Reverses the Doxorubicin-Resistance in Hepatocellular Carcinoma Cells through Regulating the Tumor Metabolism.PloS one · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesMany cancer cells show significant resistance to drugs that kill drug sensitive cancer cells and non-tumor cells and such resistance might be a consequence of the difference in metabolism. Therefore, studying the metabolism of drug resistant cancer cells and comparison with drug sensitive and normal cell lines is the objective of this research. MATERIAL AND
methodsMetabolism of cisplatin resistant and sensitive A2780 epithelial ovarian cancer cells and normal ovarian epithelium has been studied using a generic human genome-scale metabolic model and transcription data.
resultThe results demonstrate that the most different metabolisms belong to resistant and normal models, and the different reactions are involved in various metabolic pathways. However, large portion of distinct reactions are related to extracellular transport for three cell lines. Capability of metabolic models to secrete lactate was investigated to find the origin of Warburg effect. Computational results introduced SLC25A10 gene, which encodes mitochondrial dicarboxylate transporter involved in exchanging of small metabolites across the mitochondrial membrane that may play key role in high growing capacity of sensitive and resistant cancer cells. The metabolic models were also used to find single and combinatorial targets that reduce the cancer cells growth. Effect of proposed target genes on growth and oxidative phosphorylation of normal cells were determined to estimate drug side-effects.
conclusionThe deletion results showed that although the cisplatin did not cause resistant cancer cells death, but it shifts the cancer cells to a more vulnerable metabolism.
Indexed as
Identifiers
25945240PMC4414993W2155739946What OpenQuestion holds
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