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c-Src activation through a TrkA and c-Src interaction is essential for cell proliferation and hematological malignancies\

Authors
Kim, Min SooKim, Gyoung MiChoi, Yun-JeongKim, Hye JoungKim, Yoo-JinJin, Wook
Issue Date
15-Nov-2013
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Keywords
TrkA; Hematological malignancies; c-Src; PLK-1; Twist-1
Citation
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.441, no.2, pp.431 - 437
Journal Title
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume
441
Number
2
Start Page
431
End Page
437
URI
https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/14120
DOI
10.1016/j.bbrc.2013.10.082
ISSN
0006-291X
Abstract
Although the kinase receptor TrkA may play an important role in acute myeloid leukemia (AML), its involvement in other types of leukemia has not been reported. Furthermore, how it contributes to leukemogenesis is unknown. Here, we describe a molecular network that is important for TrkA function in leukemogenesis. We found that TrkA is frequently overexpressed in other types of leukemia such as acute lymphoblastic leukemia (ALL), chronic myelogenous leukemia (CML), and myelodysplastic syndrome (MDS) including AML. In addition, TrkA was overexpressed in patients with MDS or secondary AML evolving from MDS. TrkA induced significant hematological malignancies by inducing PLK-1 and Twist-1, and enhanced survival and proliferation of leukemia, which was correlated with activation of the phosphatidylinositol 3-kinase/Akt/mTOR pathway. Moreover, endogenous TrkA associated with c-Src complexes was detected in leukemia. Suppression of c-Src activation by TrkA resulted in markedly decreased expression of PLK-1 and Twist-1 via suppressed activation of Akt/mTOR cascades. These data suggest that TrkA plays a key role in leukemogenesis and reveal an unexpected physiological role for TrkA in the pathogenesis of leukemia. These data have important implications for understanding various hematological malignancies. (C) 2013 Elsevier Inc. All rights reserved.
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