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PML-RARα stabilized by zinc in human acute promyelocytic leukemia NB4 cells.

Abstract：

:Acute promyelocytic leukemia (APL) is characterized and driven by the promyelocytic leukemia protein-retinoic acid receptor alpha (PML-RARα) fusion gene. Previous studies have highlighted the importance of PML-RARα degradation in the treatment against APL. Considering the presence of two zinc fingers in the PML-RARα fusion protein, we explored the function of zinc homeostasis in maintaining PML-RARα stability. We demonstrated for the first time that zinc depletion by its chelator N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN) triggered PML-RARα degradation in NB4 APL cells via the proteasome pathway rather than the autophagy-lysosomal pathway. In contrast, autophagy protected TPEN-mediated PML-RARα degradation in NB4 APL cells. We further demonstrated that crosstalk between zinc homeostasis and nitric oxide pathway played a key role in maintaining PML-RARα stability in NB4 APL cells. These results demonstrate that zinc homeostasis is vital for maintaining PML-RARα stability, and zinc depletion by TPEN may be useful as a potential strategy to trigger PML-RARα degradation in APL cells. We also found that TPEN triggered apoptosis of NB4 APL cells in a time-dependent manner. The relationship between PML-RARα degradation and apoptosis triggered by TPEN deserves further study.

journal_name

J Inorg Biochem

journal_title

Journal of inorganic biochemistry

authors

Zhu B,Wang JY,Zhou JJ,Zhou F,Cheng W,Liu YT,Wang J,Chen X,Chen DH,Luo L,Hua ZC

doi

10.1016/j.jinorgbio.2017.07.007

subject

Has Abstract

pub_date

2017-10-01 00:00:00

pages

92-100

eissn

0162-0134

issn

1873-3344

pii

S0162-0134(17)30159-9

journal_volume

175

pub_type

杂志文章

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