Research Papers:

Amyloid precursor like protein-1 promotes JNK-mediated cell migration in Drosophila

Xingjun Wang _, Ying Sun, Shilong Han, Chenxi Wu, Yeqing Ma, Yu Zhao, Yingyao Shao, Yujun Chen, Lingzhi Kong, Wenzhe Li, Fan Zhang and Lei Xue

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Oncotarget. 2017; 8:49725-49734. https://doi.org/10.18632/oncotarget.17681

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Xingjun Wang1,*, Ying Sun1,*, Shilong Han1, Chenxi Wu2, Yeqing Ma1, Yu Zhao1, Yingyao Shao1, Yujun Chen1, Lingzhi Kong3, Wenzhe Li1, Fan Zhang3 and Lei Xue1

1Department of Interventional Radiology, Shanghai 10th People’s Hospital, Shanghai Key Laboratory of Signaling and Diseases Research, School of Life Science and Technology, Tongji University, Shanghai 200092, China

2College of Chinese Medicine, North China University of Science and Technology, Tangshan 063210, China

3Clinical Translational Research Center, Shanghai Pulmonary Hospital, School of Life Science and Technology, Tongji University, Shanghai 200092, China

*These authors have contributed equally to this work

Correspondence to:

Xingjun Wang, email: [email protected]

Lei Xue, email: [email protected]

Keywords: APLP1, cell migration, Drosophila, JNK

Received: May 18, 2015     Accepted: April 20, 2017     Published: May 08, 2017


The amyloid precursor like protein-1 (APLP1) is a member of the amyloid precursor protein (APP) family in mammals. While many studies have been focused on the pathologic role of APP in Alzheimer’s disease, the physiological functions of APLP1 have remained largely elusive. Here we report that ectopic expression of APLP1 in Drosophila induces cell migration, which is suppressed by the loss of JNK signaling and enhanced by the gain of JNK signaling. APLP1 activates JNK signaling through phosphorylation of JNK, which up-regulates the expression of matrix metalloproteinase MMP1 required for basement membranes degradation and promotes actin remodeling essential for cell migration. Our data thus provide the first in vivo evidence for a cell-autonomous role of APLP1 protein in migration.

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