Research Papers:

Alternative promotion and suppression of metastasis by JNK2 governed by its phosphorylation

Sike Hu, Xiaoli Dong, Wenjuan Gao, Dwayne Stupack, Yanhua Liu, Rong Xiang and Na Li _

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Oncotarget. 2017; 8:56569-56581. https://doi.org/10.18632/oncotarget.17507

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Sike Hu1, Xiaoli Dong1, Wenjuan Gao1, Dwayne Stupack2, Yanhua Liu1,3, Rong Xiang1,3,4 and Na Li1,3,4

1School of Medicine, Nankai University, Tianjin 300071, China

2Department of Reproductive Medicine, Division of Gynecologic Oncology, Moores Cancer Center, University of California San Diego, La Jolla, CA 92093-0987, United States

3 Tianjin Key Laboratory of Tumour Microenvironment and Neurovascular Regulation, Tianjin 300071, China

4Collaborative Innovation Center for Biotherapy, Nankai University, Tianjin 300071, China

Correspondence to:

Na Li, email: [email protected]

Rong Xiang, email: [email protected]

Keywords: JNK2, p-JNK2, Fra1, EMT

Received: December 21, 2016    Accepted: March 30, 2017    Published: April 28, 2017


Fos-related antigen 1 (Fra1) has been proposed as a gatekeeper of the mesenchymal-epithelial transition to epithelial-mesenchymal transition. Here, we showed that de-phosphorylated JNK2 increased the expression of Fra1 by promoting the expression of c-Jun and Jun-B. Conversely, phosphorylated JNK2 suppressed its expression via enhancing the ubiquitination of c-Jun and Jun-B. These data provided insights into the regulatory mechanism of JNK2 on the expression of Fra1. Our study thus demonstrated that the conversion of JNK2 from its phosphorylation to de-phosphorylation status promoted the switch of breast cancer cells from mesenchymal-epithelial transition to epithelial-mesenchymal transition.

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