NDLI: CD72 regulates the growth of KIT-mutated leukemia cell line Kasumi-1

Content Provider	PubMed Central
Author	Kataoka, Tatsuki R. Atsushi, Kumanogoh Hirata, Masahiro Moriyoshi, Koki Ueshima, Chiyuki Kawahara, Masahiro Tsuruyama, Tatsuaki Haga, Hironori
Copyright Year	2013
Abstract	Gain-of-function mutations in KIT, a member of the receptor type tyrosine kinases, are observed in certain neoplasms, including mast cell tumors (MCTs) and acute myelogenous leukemias (AMLs). A MCT line HMC1.2 harboring the KIT mutation was reported to express CD72, which could suppress the cell proliferation. Here, we examined the ability of CD72 to modify the growth of AMLs harboring gain-of-function KIT mutations. CD72 was expressed on the surface of the AML cell line, Kasumi-1. CD72 ligation by an agonistic antibody BU40 or by a natural ligand CD100, suppressed the proliferation of the Kasumi-1 cells and enhanced cell death, as monitored by caspase-3 cleavage. These responses were associated with the phosphorylation of CD72, the formation of the CD72 - SHP-1 complex and dephosphorylation of src family kinases and JNK. Thus, these results seemed to suggest that CD72 was the therapeutic potential for AML, as is the case of MCTs.
Related Links	http://dx.doi.org/10.1038/srep02861
Starting Page	2861
File Format	PDF
ISSN	20452322
e-ISSN	20452322
Journal	Scientific Reports
Volume Number	3
Language	English
Publisher	Nature Publishing Group
Publisher Date	2013-10-01
Access Restriction	Open
Rights Holder	Nature Publishing Group
Subject Keyword	Science and technology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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CD72 regulates the growth of KIT-mutated leukemia cell line Kasumi-1

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