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Open AccessArticle

SP600125 Induces Src and Type I IGF Receptor Phosphorylation Independent of JNK

State Key Laboratory of Biotherapy, Section of Oncogene, West China Hospital, Sichuan University, Chengdu 610041, China
Laboratory of Stem Cell Biology, West China Hospital, Sichuan University, Chengdu 610041, China
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2014, 15(9), 16246-16256;
Received: 15 July 2014 / Revised: 27 August 2014 / Accepted: 1 September 2014 / Published: 15 September 2014
(This article belongs to the Special Issue Signalling Molecules and Signal Transduction in Cells 2014)
c-Jun N-terminal kinases (JNK) are members of the mitogen-activated protein kinase (MAPK) family that have important roles in signal transduction. The small molecule SP600125 is widely used in biochemical studies as a JNK inhibitor. However, recent studies indicate that SP600125 may also act independent of JNK. Here, we report that SP600125 can induce Src, type I insulin-like growth factor receptor (IGF-IR), Akt and Erk1/2 phosphorylation. Notably, these effects are independent of its inhibition of JNK. Inhibition of Src abrogates the stimulation of IGF-IR, Akt and Erk1/2 phosphorylation. IGF-IR knockdown blunts the induction of both Akt and Erk1/2 phosphorylation by SP600125. Moreover, combination of SP600125 and the Src inhibitor saracatinib synergistically inhibits cell proliferation. We conclude that SP600125 can activate Src-IGF-IR-Akt/Erk1/2 signaling pathways independent of JNK. View Full-Text
Keywords: SP600125; JNK; Src; IGF-IR SP600125; JNK; Src; IGF-IR
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Kong, Q.; Hua, H.; Cui, A.; Shao, T.; Song, P.; Jiang, Y. SP600125 Induces Src and Type I IGF Receptor Phosphorylation Independent of JNK. Int. J. Mol. Sci. 2014, 15, 16246-16256.

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