Open AccessMYO10 contributes to the malignant phenotypes of colorectal cancer via RACK1 by activating integrin/Src/ FAK signaling
Author(s) -
Ou Haibin,
Wang Lili,
Xi Ziyao,
Shen Hui,
Jiang Yaofei,
Zhou Fuxiang,
Liu Yu,
Zhou Yunfeng
Publication year - 2022
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.15519
Subject(s) - metastasis , proto oncogene tyrosine protein kinase src , cancer research , integrin , downregulation and upregulation , colorectal cancer , focal adhesion , signal transduction , cancer , ubiquitin , cell migration , microbiology and biotechnology , biology , medicine , cell , biochemistry , genetics , gene
Liver metastases still remain a major cause of colorectal cancer (CRC) patient death. MYO10 is upregulated in several tumor types; however, its significance and the underlying mechanism in CRC are not entirely clear. Here, we found that MYO10 was highly expressed in CRC tumor tissues, especially in liver metastasis tissues. MYO10 knockout reduced CRC cell proliferation, invasion, and migration in vitro and CRC metastasis in vivo. We identified RACK1 by LC‐MS/MS and demonstrated that MYO10 interacts with and stabilizes RACK1. Mechanistically, MYO10 promotes CRC cell progression and metastasis via ubiquitination‐mediated RACK1 degradation and integrin/Src/FAK signaling activation. Therefore, the MYO10/RACK1/integrin/Src/FAK axis may play an important role in CRC progression and metastasis.