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A potential role of fetal hemoglobin in the development of multidrug resistance.

Abstract：

:Our previous data from a human leukemic cell line made resistant to the nucleoside analog (NA) 9-β-D-arabinofuranosylguanine (AraG) revealed a massive upregulation of fetal hemoglobin (HbF) genes and the ABCB1 gene coding for the multidrug resistance P-glycoprotein (P-gp). The expression of these genes is regulated through the same mechanisms, with activation of the p38-MAPK pathway and inhibition of methylation making transcription factors more accessible to activate these genes. We could show that AraG, as well as other NAs, and P-gp substrates could induce global DNA demethylation and induction of Hbγ and P-gp both at the mRNA and protein expression level. We speculate that the expression of HbF prior to drug exposure or in drug-resistant cell lines is a strategy of the cancer to gain more oxygen, and thereby survival benefits. We also believe that P-gp may be induced in order to excrete Hb degradation products from the cells that would otherwise be toxic. By using Hbγ siRNA and pharmacological inhibitors of HbF production we here present a possible relationship between HbF induction and multi-drug resistance in a human leukemia cell line model.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Fyrberg A,Skoglund K,Wolk M,Lotfi K

doi

10.1016/j.bbrc.2012.07.129

subject

Has Abstract

pub_date

2012-10-26 00:00:00

pages

456-60

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(12)01436-2

journal_volume

427

pub_type

杂志文章

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