FYN is required for ARHGEF16 to promote proliferation and migration in colon cancer cells

ARHGEF16 is a recently identified Rho-family guanine nucleotide exchange factor (GEF) that has been implicated in the activation of Rho-family GTPases such as Rho G, Rac, and Cdc42. However, its functions in colon cancer cell proliferation and migration are not well understood. In this study, we sho...

Full description

Saved in:
Bibliographic Details
Published in:Cell death & disease 2020-08, Vol.11 (8), p.652-652, Article 652
Main Authors: Yu, Bei, Xu, Linlin, Chen, Limin, Wang, Yao, Jiang, Hongying, Wang, Yiting, Yan, Yehong, Luo, Shiwen, Zhai, Zhenyu
Format: Article
Language:English
Subjects:
13
13/109
13/51
13/89
13/95
38/1
38/111
38/77
38/90
631/67/395
692/699/1503
82
82/80
96
96/63
Adult
Aged
Antibodies
Biochemistry
Biomedical and Life Sciences
cdc42 GTP-Binding Protein - metabolism
Cdc42 protein
Cell Biology
Cell Culture
Cell growth
Cell migration
Cell Movement - genetics
Cell proliferation
Cell Proliferation - genetics
China
Colon cancer
Colonic Neoplasms - genetics
Colonic Neoplasms - metabolism
Colorectal cancer
Female
Fyn protein
Guanine
Guanine nucleotide exchange factor
Guanine Nucleotide Exchange Factors - genetics
Guanine Nucleotide Exchange Factors - metabolism
Humans
Immunology
Kinases
Life Sciences
Male
Middle Aged
Protein Binding
Protein-tyrosine kinase
Proto-Oncogene Proteins c-fyn - genetics
Proto-Oncogene Proteins c-fyn - metabolism
rho GTP-Binding Proteins - metabolism
Signal Transduction - genetics
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:ARHGEF16 is a recently identified Rho-family guanine nucleotide exchange factor (GEF) that has been implicated in the activation of Rho-family GTPases such as Rho G, Rac, and Cdc42. However, its functions in colon cancer cell proliferation and migration are not well understood. In this study, we showed that ARHGEF16 was highly expressed in clinical specimens of colon cancer. In colon cancer cells, ARHGEF16-stimulated proliferation and migration in vitro and in vivo. Furthermore, we identified a nonreceptor tyrosine kinase, FYN, as a novel partner of ARHGEF16. Knocking down FYN expression decreased ARHGEF16 protein level in colon cancer cells. We further demonstrated that ARHGEF16-induced colon cancer cell proliferation and migration were dependent on FYN since knockdown FYN abolished the ARHGEF16-induced proliferation and migration of colon cancer cells. The FYN-ARHGEF16 axis mediates colon cancer progression and is a potential therapeutic target for colon cancer treatment.
ISSN:2041-4889
2041-4889
DOI:10.1038/s41419-020-02830-1