Interaction between granulin A and enolase 1 attenuates the migration and invasion of human hepatoma cells
Metrics: PDF 663 views | HTML 960 views | ?
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
Xiukun Lin, email: firstname.lastname@example.org
Keywords: enolase 1, granulin A, invasion, migration, protein-protein interaction
Received: December 23, 2016 Accepted: March 06, 2017 Published: March 17, 2017
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.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.