Chlorpromazine eliminates acute myeloid leukemia cells by perturbing subcellular localization of FLT3-ITD and KIT-D816V.


Journal

Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555

Informations de publication

Date de publication:
18 08 2020
Historique:
received: 21 08 2018
accepted: 13 07 2020
entrez: 20 8 2020
pubmed: 20 8 2020
medline: 17 9 2020
Statut: epublish

Résumé

Mutated receptor tyrosine kinases (MT-RTKs) such as internal tandem duplication of FMS-like tyrosine kinase 3 (FLT3 ITD) and a point mutation KIT D816V are driver mutations for acute myeloid leukemia (AML). Clathrin assembly lymphoid myeloid leukemia protein (CALM) regulates intracellular transport of RTKs, however, the precise role for MT-RTKs remains elusive. We here show that CALM knock down leads to severely impaired FLT3 ITD- or KIT D814V-dependent cell growth compared to marginal influence on wild-type FLT3- or KIT-mediated cell growth. An antipsychotic drug chlorpromazine (CPZ) suppresses the growth of primary AML samples, and human CD34

Identifiants

pubmed: 32811837
doi: 10.1038/s41467-020-17666-8
pii: 10.1038/s41467-020-17666-8
pmc: PMC7434901
doi:

Substances chimiques

Antineoplastic Agents 0
Monomeric Clathrin Assembly Proteins 0
PICALM protein, human 0
FLT3 protein, human EC 2.7.10.1
Proto-Oncogene Proteins c-kit EC 2.7.10.1
fms-Like Tyrosine Kinase 3 EC 2.7.10.1
Chlorpromazine U42B7VYA4P

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

4147

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Auteurs

Shinya Rai (S)

Department of Hematology and Rheumatology, Kindai University Faculty of Medicine, Osaka-sayama, Osaka, Japan.

Hirokazu Tanaka (H)

Department of Hematology and Rheumatology, Kindai University Faculty of Medicine, Osaka-sayama, Osaka, Japan. htanaka@med.kindai.ac.jp.

Mai Suzuki (M)

Division of Hematological Malignancy, National Cancer Center Research Institute, Chuo, Tokyo, Japan.

J Luis Espinoza (JL)

Department of Hematology and Rheumatology, Kindai University Faculty of Medicine, Osaka-sayama, Osaka, Japan.

Takahiro Kumode (T)

Department of Hematology and Rheumatology, Kindai University Faculty of Medicine, Osaka-sayama, Osaka, Japan.

Akira Tanimura (A)

Department of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.

Takafumi Yokota (T)

Department of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.

Kenji Oritani (K)

Department of Hematology, International University of Health and Welfare, Narita, Chiba, Japan.

Toshio Watanabe (T)

Department of Biological Science, Graduate School of Humanities and Sciences, Nara Women's University, Nara, Nara, Japan.

Yuzuru Kanakura (Y)

Department of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.

Itaru Matsumura (I)

Department of Hematology and Rheumatology, Kindai University Faculty of Medicine, Osaka-sayama, Osaka, Japan.

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Classifications MeSH