Oncotarget

Research Papers:

Interaction between granulin A and enolase 1 attenuates the migration and invasion of human hepatoma cells

Xiaoliang Chen, Huanli Xu, Ning Wu, Xiujun Liu, Gan Qiao, Shuonan Su, Ye Tian, Ru Yuan, Cong Li, Xiaohui Liu and Xiukun Lin _

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Oncotarget. 2017; 8:30305-30316. https://doi.org/10.18632/oncotarget.16328

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Abstract

Xiaoliang Chen1, Huanli Xu1, Ning Wu2, Xiujun Liu3, Gan Qiao1, Shuonan Su1, Ye Tian1, Ru Yuan1, Cong Li1, Xiaohui Liu1, Xiukun Lin1

1Department of Pharmacology, Capital Medical University, Beijing 100069, China

2Institute of Oceanology, Chinese Academy of Science, Qingdao 266003, China

3Institute of Medicinal Biotechnology, Chinese Academy of Medical Science, Beijing 100050, China

Correspondence to:

Xiukun Lin, email: xiukunlin@126.com

Keywords: enolase 1, granulin A, invasion, migration, protein-protein interaction

Received: December 23, 2016     Accepted: March 06, 2017     Published: March 17, 2017

ABSTRACT

Granulin A (GRN A), a peptide with a molecular 6 kDa, is derived from proteolysis of progranulin (PGRN). Previous study in our laboratory has shown that GRN A is able to inhibit cancer cell growth significantly. In the present study, we confirmed that GRN A can bind to α-enolase (ENO1) specifically as analyzed using Pull-down/MS approaches. The interaction of GRN A with ENO1 was further confirmed by Western blotting and Surface plasmon resonance (SPR) analysis. Treatment of human HepG-2 cells with GRN A inhibited cancer cell growth as well as migration and invasion of cancer cells as analyzed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazoliumbromide (MTT) and Scratch wound healing assay as well as Transwell experiments. Additionally, GRN A treatment results in augmentation of glucose uptake in cancer cells. Further study reveals that higher expression of ENO1 reversed the inhibitory effects of GRN A on migration and invasion of HepG-2 cells. The increase of glucose uptake, as well as the expression of apoptosis-related genes, is also reversed in cells overexpressing ENO1. The study provides solid evidence that there is the interaction between GRN A and ENO1 and the interaction is responsible for the effects of GRN A on glucose uptake as well as cancer cell migration and invasion.


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