GALNT2 promotes invasiveness of colorectal cancer cells partly through AXL
Journal
Molecular oncology
Journal Volume
17
Journal Issue
1
Date Issued
2023-01
Author(s)
Liao, Ying-Yu
Chuang, Ya-Ting
Lin, Hsuan-Yu
Hsu, Tzu-Wen
Hsieh, Szu-Chia
Chen, Syue-Ting
Yang, Hung-Jen
Abstract
GalNAc-type O-glycosylation and its initiating GalNAc transferases (GALNTs) play crucial roles in a wide range of cellular behaviors. Among 20 GALNT members, GALNT2 is consistently associated with poor survival of patients with colorectal cancer in public databases. However, its clinicopathological significance in colorectal cancer remains unclear. In this study, immunohistochemistry showed that GALNT2 was overexpressed in colorectal tumors compared with the adjacent nontumor tissues. GALNT2 overexpression was associated with poor survival of colorectal cancer patients. Forced expression of GALNT2 promoted migration and invasion as well as peritoneal metastasis of colorectal cancer cells. In contrast, GALNT2 knockdown with siRNAs or knockout with CRISPR/Cas9 system suppressed these malignant properties. Interestingly, we found that GALNT2 modified O-glycans on AXL and determined AXL levels via the proteasome-dependent pathway. In addition, the GALNT2-promoted invasiveness was significantly reversed by AXL siRNAs. These findings suggest that GALNT2 promotes colorectal cancer invasion at least partly through AXL.
Subjects
AXL
GALNT
glycosylation
invasion
SDGs
Publisher
WILEY
Type
journal article