ArticleOncology letters2017
The lipid metabolism gene FTO influences breast cancer cell energy metabolism via the PI3K/AKT signaling pathway.
Article in Oncology letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed.
- Regulatory roles of N6-methyladenosine methylation factors in melanoma invasion and metastasis (Review).Oncology letters · 2026Review
- Overexpression of FTO ameliorates chronic glomerulonephritis by inhibiting glycolysis in glomerular mesangial cells associated with ADPGK mNaunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Multidimensional risk impact of obesity on breast cancer incidence, treatment, and prognosis.International journal of obesity (2005) · 2026Review
- Methylation marks breast cancer metastasis: The roles of mThe Journal of biological chemistry · 2026Review
- The influence of TC0668 on glycometabolism modulation inMicrobiology spectrum · 2025Article
- Acid phosphatase type 6 promotes endometrial cancer progression via activating PI3K/AKT pathway.Molecular biology reports · 2025Article
- White Adipocyte Stem Cell Expansion Through Infant Formula Feeding: New Insights into Epigenetic Programming Explaining the Early Protein Hypothesis of Obesity.International journal of molecular sciences · 2025Review
- Article
- Identification of key LncRNAs and mRNAs associated with intramuscular fat in pig via WGCNA.BMC genomics · 2025Article
- Glycolysis modulation: New therapeutic strategies to improve pulmonary hypertension (Review).International journal of molecular medicine · 2024Review
- Functions and mechanisms of RNA mInternational journal of oncology · 2024Review
- Insights into the mCell & bioscience · 2024Review
- Treatment of Donor Cells with Oxidative Phosphorylation Inhibitor CPI Enhances Porcine Cloned Embryo Development.Animals : an open access journal from MDPI · 2024Article
- The m6A methyltransferase METTL5 promotes neutrophil extracellular trap network release to regulate hepatocellular carcinoma progression.Cancer medicine · 2024Article
- Insights into N6-methyladenosine (m6A) modification of noncoding RNA in tumor microenvironment.Aging · 2023Review
- Oncogenic metabolic reprogramming in breast cancer: focus on signaling pathways and mitochondrial genes.Medical oncology (Northwood, London, England) · 2023Review
- m6A readers, writers, erasers, and the m6A epitranscriptome in breast cancer.Journal of molecular endocrinology · 2023Review
- Article
- Crosstalk between N6-methyladenosine (m6A) modification and noncoding RNA in tumor microenvironment.International journal of biological sciences · 2023Review
- Unraveling the Complex Interactions between the Fat Mass and Obesity-Associated (FTO) Gene, Lifestyle, and Cancer.Advances in nutrition (Bethesda, Md.) · 2022Review
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study assessed the effect of the lipid metabolism, fat mass and the obesity-associated gene (FTO), on energy metabolism of breast cancer cells. The human breast cancer cell lines, MCF-7 and MDA-MB-231, and HCC1937 human breast cells were studied. Real-time PCR was used to measure the levels of FTO mRNA from breast cancer cells and normal breast cells. MDA-MB-231 cells were transfected with miFTO inhibitor or inhibitor control, and cells were assessed for levels of lactic acid, ATP, pyruvate kinase activity, and hexokinase activity assay using specific kits. Western blot analysis was used to measure the levels of phosphatidylinositol 3-kinase (PI3K), p-PI3K, protein kinase B (Akt) and p-Akt in transfected breast cancer cells. The expression of FTO was significantly increased in MCF-7 and MDA-MB-231 cells compared with HCC1937 cells (P<0.01). The lactic acid content of breast cancer cells transfected with the miFTO inhibitor was significantly lower compared with cells transfected with the miFTO inhibitor control and nontransfected cells (P<0.05). The ATP content of breast cancer cells transfected with the miFTO inhibitor was significantly lower compared with the control group and inhibitor control group (P<0.05). The pyruvate kinase activity and hexokinase activity of breast cancer cells transfected with the miFTO inhibitor were significantly lower compared with the control group and inhibitor control group (P<0.01). Western blot analysis showed that after breast cancer cells were transfected with the miFTO inhibitor, the levels of PI3K, p-PI3K, Akt and p-Akt were significantly lower than in the control group and inhibitor control group. In conclusion, the FTO gene is overexpressed in breast cancer cells. Overexpression of the FTO gene can promote breast cancer cell glycolysis and the mechanism is related to the PI3K/AKT signaling pathway.
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