ETV6-NTRK3 as a therapeutic target of small molecule inhibitor PKC412

被引：43
|
作者：
Hoang Thanh Chi [1 ]
Bui Thi Kim Ly
Kano, Yasuhiko
Tojo, Arinobu [2 ]
Watanabe, Toshiki
Sato, Yuko [3 ]
机构：
[1] Univ Tokyo, Dept Med Genome Sci, Grad Sch Frontier Sci, Minato Ku, Tokyo 1088639, Japan
[2] Univ Tokyo, Inst Med Sci, Res Hosp, Div Mol Therapy,Dept Hematol Oncol, Tokyo 1088639, Japan
[3] Musashimurayama Hosp, Tokyo 2080011, Japan
来源：
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2012年 / 429卷 / 1-2期
关键词：
AML; ETV6-NTRK3; PKC412; IMS-M2; M0-91; ACUTE MYELOID-LEUKEMIA; ACUTE LYMPHOBLASTIC-LEUKEMIA; ACUTE MYELOGENOUS LEUKEMIA; PROTEIN-TYROSINE KINASE; SIGNAL-TRANSDUCTION; GENE FUSION; CONGENITAL FIBROSARCOMA; CELL-LINE; NEUROTROPHIN RECEPTORS; MESOBLASTIC NEPHROMA;
D O I：
10.1016/j.bbrc.2012.10.087
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
The ETV6-NTRK3 (EN) fusion gene which encodes a chimeric tyrosine kinase was first identified by cloning of the t(12;15)(p13;q25) translocation in congenital fibrosarcoma (CFS). Since then, EN has been also found in congenital mesoblastic nephroma (CMN), secretory breast carcinoma (SBC) and acute myelogenous leukemia (AML). Using IMS-M2 and M0-91 cell lines harboring the EN fusion gene, and Ba/F3 cells stably transfected with EN, we demonstrated that PKC412, also known as midostaurin, is an inhibitor of EN. Inhibition of EN activity by PKC412 suppressed the activity of it downstream molecules leading to inhibition of cell proliferation and induction of apoptosis. Our data for the first time suggested that PKC412 could serve as therapeutic drug for treatment of patients with this fusion. (C) 2012 Elsevier Inc. All rights reserved.
引用
收藏
页码：87 / 92
页数：6
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