Pharmacological or genetic inhibition of hypoxia signaling attenuates oncogenic RAS-induced cancer phenotypes.


Journal

Disease models & mechanisms
ISSN: 1754-8411
Titre abrégé: Dis Model Mech
Pays: England
ID NLM: 101483332

Informations de publication

Date de publication:
01 02 2022
Historique:
received: 03 02 2021
accepted: 18 09 2021
pubmed: 29 9 2021
medline: 1 4 2022
entrez: 28 9 2021
Statut: ppublish

Résumé

Oncogenic Ras mutations are highly prevalent in hematopoietic malignancies. However, it is difficult to directly target oncogenic RAS proteins for therapeutic intervention. We have developed a Drosophila acute myeloid leukemia model induced by human KRASG12V, which exhibits a dramatic increase in myeloid-like leukemia cells. We performed both genetic and drug screens using this model. The genetic screen identified 24 candidate genes able to attenuate the oncogenic RAS-induced phenotype, including two key hypoxia pathway genes HIF1A and ARNT (HIF1B). The drug screen revealed that echinomycin, an inhibitor of HIF1A, can effectively attenuate the leukemia phenotype caused by KRASG12V. Furthermore, we showed that echinomycin treatment can effectively suppress oncogenic RAS-driven leukemia cell proliferation, using both human leukemia cell lines and a mouse xenograft model. These data suggest that inhibiting the hypoxia pathway could be an effective treatment approach and that echinomycin is a promising targeted drug to attenuate oncogenic RAS-induced cancer phenotypes. This article has an associated First Person interview with the first author of the paper.

Identifiants

pubmed: 34580712
pii: 272327
doi: 10.1242/dmm.048953
pmc: PMC8617310
pii:
doi:

Substances chimiques

Echinomycin 512-64-1

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : NIAID NIH HHS
ID : R01 AI064350
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK098410
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL134940
Pays : United States

Informations de copyright

© 2021. Published by The Company of Biologists Ltd.

Déclaration de conflit d'intérêts

Competing interests The authors declare no competing or financial interests.

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Auteurs

Jun-Yi Zhu (JY)

Center for Precision Disease Modeling, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Division of Immunotherapy, University of Maryland School of Medicine, Baltimore, MD 21201, USA.

Xiaohu Huang (X)

Center for Precision Disease Modeling, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Division of Immunotherapy, University of Maryland School of Medicine, Baltimore, MD 21201, USA.

Yulong Fu (Y)

Center for Precision Disease Modeling, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD 21201, USA.

Yin Wang (Y)

Division of Endocrinology, Diabetes and Nutrition, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD 21201, USA.

Pan Zheng (P)

Division of Endocrinology, Diabetes and Nutrition, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD 21201, USA.

Yang Liu (Y)

Division of Endocrinology, Diabetes and Nutrition, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD 21201, USA.

Zhe Han (Z)

Center for Precision Disease Modeling, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Division of Immunotherapy, University of Maryland School of Medicine, Baltimore, MD 21201, USA.

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