Expression of Mitochondrial Ferritin in K562 Leukemic Cell During ATRA-induced Cell Differentiation
10.3969/j.issn.1672-173X.2010.01.017
- VernacularTitle:全反式维甲酸诱导K562细胞分化过程中线粒体铁蛋白表达的研究
- Author:
Lei SUN
1
;
Ga LIAO
;
Ju GAO
;
Ting-Ting CHEN
;
Lin-Li PAN
;
Li-Xing YUAN
Author Information
1. 四川大学华西第四医院
- Keywords:
ATRA;
K562 leukemic cell;
Mitochondrial ferritin;
Transferrin receptor 1;
Ferritin
- From:
Journal of Sichuan University (Medical Sciences)
2010;41(1):77-80,90
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the expression of MtF,transferrin receptor 1(TfR1)and ferritin(Fn)mRNAs in K562 leukemic cells during ATRA-induced cell differentiation and to explore the interrelationship between the expression levels of these iron metabolism-related molecules.Methods K562 cells cultured with or without ATRA(1 μmol/L)were collected at 24.72 and 120 hours respectively.Cell differentiation toward granulocyte lineage was confirmed by microscopic study(Wright's staining)and flowcytometry.Expression levels of MtF,TfR1 and Fn were evaluated with semiquantitative RT-PCR,while K562 cells cultured without ATRA as control.Results Over 21.2%of K562 cells demonstrated features of granulocyte,and the expression of CD13 on cell surface increased significantly at day 5 with ATRA treatment(P＜0.05,compared with control).K562 cells could express a certain level of MtF before ATRA-induced differentiation.With increase of ATRA-induced cell differentiation,MtF mRNA expressions were downregulated progressively.After 5 days of induced cell differentiation,expression levels of MtF and TfR1 mRNA were just 86.5%and 79.2%of that before ATRA treatment.While Fn mRNA expression increased to 1.21 folds of that before ATRA treatment.Conclusion MtF expression is downregulated during ATRA-induced K562 cell differentiation,with concomitant downregulation of TfR1 and upregulation of Fn.The coordinated expression regulation of these key iron metabolism-related molecules during cell differentiation may in turn inhibit TfR1-mediated iron uptake via endocytosis and thus adversely affect cell proliferation potential.
