ArticleCellular and molecular life sciences : CMLS2015
Mitochondrial ferritin, a new target for inhibiting neuronal tumor cell proliferation.
Article in Cellular and molecular life sciences : CMLS, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- The regulation of mitochondrial ferritin on mitochondrial redox balance is essential to cell fate decision.Redox biology · 2026Review
- Mitochondrial Ferritin Overexpression Attenuates Ferroptosis and Mitochondrial Dysfunction by Reducing VDAC1 to Relieve MI/RI-Induced Damage.Journal of cellular and molecular medicine · 2025Article
- Transmembrane serine protease 6, a novel target for inhibition of neuronal tumor growth.Cell death & disease · 2024Article
- Iron and Targeted Iron Therapy in Alzheimer's Disease.International journal of molecular sciences · 2023Review
- A novel view of ferritin in cancer.Biochimica et biophysica acta. Reviews on cancer · 2023Review
- Identification and Characterization of Metabolic Subtypes of Endometrial Cancer Using a Systems-Level Approach.Metabolites · 2023Article
- Review
- Biochemistry of mammalian ferritins in the regulation of cellular iron homeostasis and oxidative responses.Science China. Life sciences · 2021Review
- FTH1 Pseudogenes in Cancer and Cell Metabolism.Cells · 2020Review
- Iron loss triggers mitophagy through induction of mitochondrial ferritin.EMBO reports · 2020Article
- Effects of FTMT Expression by Retinal Pigment Epithelial Cells on Features of Angiogenesis.International journal of molecular sciences · 2020Article
- p53 tumor suppressor and iron homeostasis.The FEBS journal · 2019Review
- Prognostic Value of Ferritin-to-Hemoglobin Ratio in Patients with Advanced Non-Small-Cell Lung Cancer.Journal of Cancer · 2019Article
- Roflumilast enhances cisplatin-sensitivity and reverses cisplatin-resistance of ovarian cancer cells via cAMP/PKA/CREB-FtMt signalling axis.Cell proliferation · 2018Article
- Differences in Gene Expression Profiles and Phenotypes of Differentiated SH-SY5Y Neurons Stably Overexpressing Mitochondrial Ferritin.Frontiers in molecular neuroscience · 2018Article
- Roflumilast restores cAMP/PKA/CREB signaling axis for FtMt-mediated tumor inhibition of ovarian cancer.Oncotarget · 2017Article
- Mitochondrial Ferritin Protects Hydrogen Peroxide-Induced Neuronal Cell Damage.Aging and disease · 2017Article
- Nasal delivery of nanoliposome-encapsulated ferric ammonium citrate can increase the iron content of rat brain.Journal of nanobiotechnology · 2017Article
- Mitochondrial ferritin protects the murine myocardium from acute exhaustive exercise injury.Cell death & disease · 2016Article
- Characterization of human mitochondrial ferritin promoter: identification of transcription factors and evidences of epigenetic control.Scientific reports · 2016Article
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial ferritin (FtMt) has a significant effect on the regulation of cytosolic and mitochondrial iron levels. However, because of the deficiency of iron regulatory elements (IRE) in FtMt's gene sequence, the exact function of FtMt remains unclear. In the present study, we found that FtMt dramatically inhibited SH-SY5Y cell proliferation and tumor growth in nude mice. Interestingly, excess FtMt did not adversely affect the development of drosophila. Additionally, we found that the expression of FtMt in human normal brain tissue was significantly higher than that of neuroblastoma, but not higher than that of neurospongioma. However, the expression of transferrin receptor 1 is completely opposite. We therefore hypothesized that increased expression of FtMt may negatively affect the vitality of neuronal tumor cells. Therefore, we further investigated the underlying mechanisms of FtMt's inhibitory effects on neuronal tumor cell proliferation. As expected, FtMt overexpression disturbed the iron homeostasis of tumor cells and significantly downregulated the expression of proliferating cell nuclear antigen. Moreover, FtMt affected cell cycle, causing G1/S arrest by modifying the expression of cyclinD1, cyclinE, Cdk2, Cdk4 and p21. Remarkably, FtMt strongly upregulated the expression of the tumor suppressors, p53 and N-myc downstream-regulated gene-1 (NDRG1), but dramatically decreased C-myc, N-myc and p-Rb levels. This study demonstrates for the first time a new role and mechanism for FtMt in the regulation of cell cycle. We thus propose FtMt as a new candidate target for inhibiting neuronal tumor cell proliferation. Appropriate regulation of FtMt expression may prevent tumor cell growth. Our study may provide a new strategy for neuronal cancer therapy.
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