GALNT2 promotes invasiveness of colorectal cancer cells partly through AXL

Ying Yu Liao; Ya Ting Chuang; Hsuan Yu Lin; Neng Yu Lin; Tzu Wen Hsu; Szu Chia Hsieh; Syue Ting Chen; Ji Shiang Hung; Hung Jen Yang; Jin Tung Liang; Min Chuan Huang; John Huang

doi:10.1002/1878-0261.13347

GALNT2 promotes invasiveness of colorectal cancer cells partly through AXL

Ying Yu Liao, Ya Ting Chuang, Hsuan Yu Lin, Neng Yu Lin, Tzu Wen Hsu, Szu Chia Hsieh, Syue Ting Chen, Ji Shiang Hung, Hung Jen Yang, Jin Tung Liang, Min Chuan Huang^*, John Huang^*

^*Corresponding author for this work

Department of Anatomy

Research output: Contribution to journal › Journal Article › peer-review

11 Scopus citations

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.

Original language	English
Pages (from-to)	119-133
Number of pages	15
Journal	Molecular Oncology
Volume	17
Issue number	1
DOIs	https://doi.org/10.1002/1878-0261.13347
State	Published - 01 2023

Bibliographical note

Keywords

AXL
GALNT
glycosylation
invasion
Neoplasm Invasiveness
Humans
Cell Line, Tumor
Colorectal Neoplasms/genetics
Glycosylation
Polypeptide N-acetylgalactosaminyltransferase
N-Acetylgalactosaminyltransferases/genetics

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1002/1878-0261.13347

Cite this

@article{006e81a6f69d4175968e5b3b19e1d45c,

title = "GALNT2 promotes invasiveness of colorectal cancer cells partly through AXL",

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.",

keywords = "AXL, GALNT, glycosylation, invasion, Neoplasm Invasiveness, Humans, Cell Line, Tumor, Colorectal Neoplasms/genetics, Glycosylation, Polypeptide N-acetylgalactosaminyltransferase, N-Acetylgalactosaminyltransferases/genetics",

author = "Liao, {Ying Yu} and Chuang, {Ya Ting} and Lin, {Hsuan Yu} and Lin, {Neng Yu} and Hsu, {Tzu Wen} and Hsieh, {Szu Chia} and Chen, {Syue Ting} and Hung, {Ji Shiang} and Yang, {Hung Jen} and Liang, {Jin Tung} and Huang, {Min Chuan} and John Huang",

note = "{\textcopyright} 2022 The Authors. Molecular Oncology published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies.",

year = "2023",

month = jan,

doi = "10.1002/1878-0261.13347",

language = "英语",

volume = "17",

pages = "119--133",

journal = "Molecular Oncology",

issn = "1574-7891",

publisher = "John Wiley and Sons Ltd",

number = "1",

}

TY - JOUR

T1 - GALNT2 promotes invasiveness of colorectal cancer cells partly through AXL

AU - Liao, Ying Yu

AU - Chuang, Ya Ting

AU - Lin, Hsuan Yu

AU - Lin, Neng Yu

AU - Hsu, Tzu Wen

AU - Hsieh, Szu Chia

AU - Chen, Syue Ting

AU - Hung, Ji Shiang

AU - Yang, Hung Jen

AU - Liang, Jin Tung

AU - Huang, Min Chuan

AU - Huang, John

PY - 2023/1

Y1 - 2023/1

N2 - 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.

AB - 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.

KW - AXL

KW - GALNT

KW - glycosylation

KW - invasion

KW - Neoplasm Invasiveness

KW - Humans

KW - Cell Line, Tumor

KW - Colorectal Neoplasms/genetics

KW - Glycosylation

KW - Polypeptide N-acetylgalactosaminyltransferase

KW - N-Acetylgalactosaminyltransferases/genetics

UR - http://www.scopus.com/inward/record.url?scp=85143966221&partnerID=8YFLogxK

U2 - 10.1002/1878-0261.13347

DO - 10.1002/1878-0261.13347

M3 - 文章

C2 - 36409270

AN - SCOPUS:85143966221

SN - 1574-7891

VL - 17

SP - 119

EP - 133

JO - Molecular Oncology

JF - Molecular Oncology

IS - 1

ER -

GALNT2 promotes invasiveness of colorectal cancer cells partly through AXL

Abstract

Bibliographical note

Keywords

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this