ArticlePhysiological reports2015
Iron depletion results in Src kinase inhibition with associated cell cycle arrest in neuroblastoma cells.
Article in Physiological reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Quantitative Proteome and Transcriptome Dynamics Analysis Reveals Iron Deficiency Response Networks and Signature in Neuronal Cells.Molecules (Basel, Switzerland) · 2022Article
- Reversing oncogenic transformation with iron chelation.Oncotarget · 2021Review
- Iron Deficiency Reprograms Phosphorylation Signaling and Reduces O-GlcNAc Pathways in Neuronal Cells.Nutrients · 2021Article
- Suppressive effects of iron chelation in clear cell renal cell carcinoma and their dependency on VHL inactivation.Free radical biology & medicine · 2019Article
- Di-2-pyridylhydrazone Dithiocarbamate Butyric Acid Ester Exerted Its Proliferative Inhibition against Gastric Cell via ROS-Mediated Apoptosis and Autophagy.Oxidative medicine and cellular longevity · 2018Article
- Iron deposition is associated with differential macrophage infiltration and therapeutic response to iron chelation in prostate cancer.Scientific reports · 2017Article
- Cytotoxic activity of expanded coordination bis-thiosemicarbazones and copper complexes thereof.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2016Article
- Iron depletion suppresses mTORC1-directed signalling in intestinal Caco-2 cells via induction of REDD1.Cellular signalling · 2016Article
- Upregulation of PP2Ac predicts poor prognosis and contributes to aggressiveness in hepatocellular carcinoma.Cancer biology & therapy · 2016Article
- BCc1, the novel antineoplastic nanocomplex, showed potent anticancer effects in vitro and in vivo.Drug design, development and therapy · 2016Article
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2 authors at 1 institution in 1 country.
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Abstract
Iron is required for cellular proliferation. Recently, using systematic time studies of neuroblastoma cell growth, we better defined the G1 arrest caused by iron chelation to a point in mid-G1, where cyclin E protein is present, but the cyclin E/CDK2 complex kinase activity is inhibited. In this study, we again used the neuroblastoma SKNSH cells lines to pinpoint the mechanism responsible for this G1 block. Initial studies showed in the presence of DFO, these cells have high levels of p27 and after reversal of iron chelation p27 is degraded allowing for CDK2 kinase activity. The initial activation of CDK2 kinase allows cells to exit G1 and enter S phase. Furthermore, we found that inhibition of p27 degradation by DFO is directly associated with inhibition of Src kinase activity measured by lack of phosphorylation of Src at the 416 residue. Activation of Src kinase occurs very early after reversal from the DFO G1 block and is temporally associated with initiation of cellular proliferation associated with entry into S phase. For the first time therefore we show that iron chelation inhibits Src kinase activity and this activity is a requirement for cellular proliferation.
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