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Published on: May 13, 2021
APLP2 Modulates JNK-Dependent Cell Migration in Drosophila
Xingjun Wang1,2, Xiaowei Guo1, Yeqing Ma1
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.
Amyloid precursor-like protein 2 (APLP2) drives cell migration in Drosophila by activating JNK signaling. This pathway increases MMP1 expression, degrading the basement membrane and promoting cell movement.
Area of Science:
- Molecular biology
- Cell biology
- Developmental biology
Background:
- Amyloid precursor-like protein 2 (APLP2) is expressed in human cells and implicated in cancer.
- The precise function of APLP2 in regulating cell migration is not fully understood.
Purpose of the Study:
- To investigate the role of APLP2 in cell migration.
- To elucidate the underlying molecular mechanisms of APLP2-mediated cell migration.
Main Methods:
- Ectopic expression of APLP2 in Drosophila.
- Analysis of JNK signaling pathway activation.
- Assessment of matrix metalloproteinase MMP1 expression.
Main Results:
- Ectopic APLP2 expression in Drosophila induces cell migration.
- JNK signaling pathway mediates APLP2-induced cell migration; JNK loss suppresses, while JNK gain enhances migration.
- APLP2 activates JNK signaling via phosphorylation, leading to MMP1 expression and basement membrane degradation.
Conclusions:
- APLP2 plays a significant role in promoting cell migration.
- The JNK signaling pathway is a key mediator of APLP2's function in cell migration.
- APLP2's activation of JNK signaling and subsequent MMP1 expression provides a mechanism for basement membrane degradation and enhanced cell motility.
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