Zinc as a potential regulator of the BCR-ABL oncogene in chronic myelocytic leukemia cells.


Journal

Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS)
ISSN: 1878-3252
Titre abrégé: J Trace Elem Med Biol
Pays: Germany
ID NLM: 9508274

Informations de publication

Date de publication:
May 2024
Historique:
received: 29 11 2023
revised: 21 01 2024
accepted: 30 01 2024
medline: 18 3 2024
pubmed: 8 2 2024
entrez: 7 2 2024
Statut: ppublish

Résumé

Generally, decreased zinc in the serum of tumor patients but increased zinc in tumor cells can be observed. However, the role of zinc homeostasis in myeloid leukemia remains elusive. BCR-ABL is essential for the initiation, maintenance, and progression of chronic myelocytic leukemia (CML). We are currently investigating the association between zinc homeostasis and CML. Genes involved in zinc homeostasis were examined using three GEO datasets. Western blotting and qPCR were used to investigate the effects of zinc depletion on BCR-ABL expression. Furthermore, the effect of TPEN on BCR-ABL promoter activity was determined using the dual-luciferase reporter assay. MRNA stability and protein stability of BCR-ABL were assessed using actinomycin D and cycloheximide. Transcriptome data mining revealed that zinc homeostasis-related genes were associated with CML progression and drug resistance. Several zinc homeostasis genes were affected by TPEN. Additionally, we found that zinc depletion by TPEN decreased BCR-ABL mRNA stability and transcriptional activity in K562 CML cells. Zinc supplementation and sodium nitroprusside treatment reversed BCR-ABL downregulation by TPEN, suggesting zinc- and nitric oxide-dependent mechanisms. Our in vitro findings may help to understand the role of zinc homeostasis in BCR-ABL regulation and thus highlight the importance of zinc homeostasis in CML.

Sections du résumé

BACKGROUND BACKGROUND
Generally, decreased zinc in the serum of tumor patients but increased zinc in tumor cells can be observed. However, the role of zinc homeostasis in myeloid leukemia remains elusive. BCR-ABL is essential for the initiation, maintenance, and progression of chronic myelocytic leukemia (CML). We are currently investigating the association between zinc homeostasis and CML.
METHODS METHODS
Genes involved in zinc homeostasis were examined using three GEO datasets. Western blotting and qPCR were used to investigate the effects of zinc depletion on BCR-ABL expression. Furthermore, the effect of TPEN on BCR-ABL promoter activity was determined using the dual-luciferase reporter assay. MRNA stability and protein stability of BCR-ABL were assessed using actinomycin D and cycloheximide.
RESULTS RESULTS
Transcriptome data mining revealed that zinc homeostasis-related genes were associated with CML progression and drug resistance. Several zinc homeostasis genes were affected by TPEN. Additionally, we found that zinc depletion by TPEN decreased BCR-ABL mRNA stability and transcriptional activity in K562 CML cells. Zinc supplementation and sodium nitroprusside treatment reversed BCR-ABL downregulation by TPEN, suggesting zinc- and nitric oxide-dependent mechanisms.
CONCLUSION CONCLUSIONS
Our in vitro findings may help to understand the role of zinc homeostasis in BCR-ABL regulation and thus highlight the importance of zinc homeostasis in CML.

Identifiants

pubmed: 38325182
pii: S0946-672X(24)00027-0
doi: 10.1016/j.jtemb.2024.127407
pii:
doi:

Substances chimiques

Fusion Proteins, bcr-abl EC 2.7.10.2
Zinc J41CSQ7QDS
N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine R9PTU1U29I
Ethylenediamines 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

127407

Informations de copyright

Copyright © 2024 Elsevier GmbH. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Bo Zhu (B)

School of Biopharmacy, China Pharmaceutical University, Nanjing 211198, PR China. Electronic address: zhubo@cpu.edu.cn.

Longshuo Sun (L)

School of Biopharmacy, China Pharmaceutical University, Nanjing 211198, PR China.

Zhonghua Li (Z)

School of Biopharmacy, China Pharmaceutical University, Nanjing 211198, PR China.

Pengyou Shang (P)

School of Biopharmacy, China Pharmaceutical University, Nanjing 211198, PR China.

Chunhao Yang (C)

School of Biopharmacy, China Pharmaceutical University, Nanjing 211198, PR China.

Kaiqiang Li (K)

School of Biopharmacy, China Pharmaceutical University, Nanjing 211198, PR China.

Jiahuang Li (J)

School of Biopharmacy, China Pharmaceutical University, Nanjing 211198, PR China.

Qi Zhi (Q)

Department of Radiology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing 210029, PR China.

Zichun Hua (Z)

School of Biopharmacy, China Pharmaceutical University, Nanjing 211198, PR China; State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing 210023, PR China. Electronic address: huazc@nju.edu.cn.

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Classifications MeSH