ArticleJournal of experimental & clinical cancer research : CR2020
MIEF2 over-expression promotes tumor growth and metastasis through reprogramming of glucose metabolism in ovarian cancer.
Article in Journal of experimental & clinical cancer research : CR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 46 citations in OpenAlex.
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- Dynamin-Related Protein 1-Dependent Disruption of Mitochondrial Homeostasis Drives Blue Light-Induced Epithelial-Mesenchymal Transition in Retinal Aging.Aging cell · 2026Article
- Subcellular Stress Markers in Epithelial Ovarian Cancer.International journal of molecular sciences · 2025Review
- Metabolic Plasticity and Cancer Stem Cell Metabolism: Exploring the Glycolysis-OXPHOS Switch as a Mechanism for Resistance and Tumorigenesis.Stem cell reviews and reports · 2025Review
- High IGFL2 regulates ovarian cancer progression and the tumor immune microenvironment via the Warburg effect.Molecular and cellular biochemistry · 2025Article
- Targeting mitochondrial structure and dynamics for therapeutic intervention in cancer.PLoS biology · 2025Article
- Mitochondrial medicine: "from bench to bedside" 3PM-guided concept.The EPMA journal · 2025Article
- PTTG1 promotes M2 macrophage polarization via the cGMP-PKG signaling pathway and facilitates EMT progression in human epithelial ovarian cancer cells.Discover oncology · 2025Article
- Identification of prognostic subtypes and the role of FXYD6 in ovarian cancer through multi-omics clustering.Frontiers in immunology · 2025Article
- The role of mitochondria in tumor metastasis and advances in mitochondria-targeted cancer therapy.Cancer metastasis reviews · 2024Review
- Mitochondrial elongation impairs breast cancer metastasis.Science advances · 2024Article
- MARCH5 promotes aerobic glycolysis to facilitate ovarian cancer progression via ubiquitinating MPC1.Apoptosis : an international journal on programmed cell death · 2024Article
- Identification and validation of IRF6 related to ovarian cancer and biological function and prognostic value.Journal of ovarian research · 2024Article
- Mechanisms of Modulation of Mitochondrial Architecture.Biomolecules · 2023Review
- Research progress on the mechanism of glycolysis in ovarian cancer.Frontiers in immunology · 2023Review
- Metformin improves depressive-like behavior in experimental Parkinson's disease by inducing autophagy in the substantia nigra and hippocampus.Inflammopharmacology · 2022Article
- Identification and validation of a 9-gene signature for the prognosis of ovarian cancer by integrated bioinformatical analysis.Annals of translational medicine · 2022Article
- Sequence Requirements for miR-424-5p Regulating and Function in Cancers.International journal of molecular sciences · 2022Review
- Quantifying the Patterns of Metabolic Plasticity and Heterogeneity along the Epithelial-Hybrid-Mesenchymal Spectrum in Cancer.Biomolecules · 2022Article
- Mitochondrial Fission and Fusion in Tumor Progression to Metastasis.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundIncreasing evidence has revealed the close link between mitochondrial dynamic dysfunction and cancer. MIEF2 (mitochondrial elongation factor 2) is mitochondrial outer membrane protein that functions in the regulation of mitochondrial fission. However, the expression, clinical significance and biological functions of MIEF2 are still largely unclear in human cancers, especially in ovarian cancer (OC).
methodsThe expression and clinical significance of MIEF2 were determined by qRT-PCR, western blot and immunohistochemistry analyses in tissues and cell lines of OC. The biological functions of MIEF2 in OC were determined by in vitro and in vivo cell growth and metastasis assays. Furthermore, the effect of MIEF2 on metabolic reprogramming of OC was determined by metabolomics and glucose metabolism analyses.
resultsMIEF2 expression was significantly increased in OC mainly due to the down-regulation of miR-424-5p, which predicts poor survival for patients with OC. Knockdown of MIEF2 significantly suppressed OC cell growth and metastasis both in vitro and in vivo by inhibiting G1-S cell transition, epithelial-to-mesenchymal transition (EMT) and inducing cell apoptosis, while forced expression of MIEF2 had the opposite effects. Mechanistically, mitochondrial fragmentation-suppressed cristae formation and thus glucose metabolism switch from oxidative phosphorylation to glycolysis was found to be involved in the promotion of growth and metastasis by MIEF2 in OC cells.
conclusionsMIEF2 plays a critical role in the progression of OC and may serve as a valuable prognostic biomarker and therapeutic target in the treatment of this malignancy.
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