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Poonam Gupta Pratibha Singh Hriday S. Pandey Pankaj Seth Chinmay K. Mukhopadhyay 《Biochimica et Biophysica Acta (BBA)/General Subjects》2019,1863(3):547-564
Background
Elevated endogenous phosphoinositide-3-kinase (PI3K) activity is critical for cell proliferation in gliomas. Iron availability is one of the essential factors for cell growth and proliferation. However, any relation between PI3K and cellular iron homeostasis has not been understood so far.Methods
Glioma cells and human primary astrocytes were treated with class I PI3K inhibitors to examine regulation of iron homeostasis components. Regulation of ferritin was detected at mRNA and translational level. Labile iron pool (LIP) and cell proliferation were examined in glioma cells and human primary astrocytes.Results
Blocking of PI3K activity elevated ferritin level by 6–10 folds in glioma cells by augmenting mRNA expression of ferritin subunits and also by influencing ferritin translation. IRE-IRP interaction was affected due to conversion of IRP1 to cytosolic aconitase that was influenced by increased iron-sulfur scaffold protein iron-sulfur cluster assembly enzyme (ISCU) level. Elevated ferritin sequestered LIP to affect cell proliferation that was reversed in silencing ferritin by siRNAs of ferritin-H and ISCU. Human primary astrocyte with little PI3K activity did not show any change in ferritin level, LIP and cell proliferation by PI3K inhibitors.Conclusions
PI3K inhibition promotes ferritin synthesis by dual mechanism resulting sequestration of iron to limit its availability for cell proliferation in glioma cells but not in primary astrocytes.General Significance: This observation establishes a relation between PI3K signalling and iron homeostasis in glioma cells. It also implies that activated PI3K controls ferritin expression to ensure availability of adequate iron required for cell proliferation. 相似文献2.
Summary Three bacteria, two of which were previously noted as active heterotrophic nitrifiers, were examined for their ability to grow and nitrify with the siderophore deferrioxamine B as the carbon source.Pseudomonas aureofaciens displayed limited growth and nitrification while a heterotrophic nitrifyingAlcaligenes sp. was without action concerning its metabolism of deferrioxamine B. The third bacterium, a unique Gram-negative soil isolate, was unable to nitrify deferrioxamine B but grew well when the siderophore was employed as the sole C source. The Gram-negative bacterium removed deferrioxamine B from the medium and left only residual amounts of the compound in solution at the termination of its growth. The organism was without action when the ferrated analogue of deferrioxamine B, ferrioxamine B, sereved as either the C source for growth, for metabolism by resting cells, or as the substrate for cell-free extracts. Deferrioxamine B, by contrast, was rapidly metabolized by resting cells. Cell-free extracts of the bacterium synthesized a monohydroxamate(s) when deferrioxamine B was the substrate. The catabolism of deferrioxamine B, which is synthesized by soil microbes, suggests that soil microflora have the ability to return deferrioxamine B, and perhaps other, siderophores to the C cycle.Abbreviations DFB
deferrioxamine B;
- FB
ferrioxamine B
- PhMeSO2F
phenylmethylsulfonyl fluoride 相似文献
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