![](/images/graphics-bg.png)
T-Synthase Deficiency Enhances Oncogenic Features in Human Colorectal Cancer Cells via Activation of Epithelial-Mesenchymal Transition
Joint Authors
Wen, Tao
An, Guangyu
Gao, Tianbo
Liu, Jian
Dong, Xichen
Jiang, Yuliang
Liu, Zhe
Source
Issue
Vol. 2018, Issue 2018 (31 Dec. 2018), pp.1-7, 7 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2018-06-21
Country of Publication
Egypt
No. of Pages
7
Main Subjects
Abstract EN
Background.
Immature truncated O-glycans such as Tn antigen are frequently detected in human colorectal cancer (CRC); however, the precise pathological consequences of Tn antigen expression on CRC are unknown.
T-synthase is the key enzyme required for biosynthesis of mature O-glycans.
Here we investigated the functional roles of Tn antigen expression mediated by T-synthase deficiency in CRC cells.
Methods.
To knock out T-synthase, we used CRISPR-Cas9 technology to target C1GALT1, the gene encoding T-synthase, in a CRC cell line (HCT116).
Deletion of T-synthase was confirmed by western blotting, and expression of Tn antigen was determined by flow cytometry in HCT116 cells.
We then assessed the biological effects of T-synthase deficiency on oncogenic behaviors in HCT116 cells.
Furthermore, we analyzed the mechanistic role of T-synthase deficiency in cancer cells by determining the epithelial-mesenchymal transition (EMT) pathway.
Results.
We showed that forced knockout of T-synthase in HCT116 cells significantly induced Tn antigen expression, which represented the occurrence of aberrant O-glycosylation.
Loss of T-synthase significantly enhanced cell proliferation and adhesion, as well as migration and invasiveness in culture.
More importantly, we demonstrated that T-synthase deficiency directly induced classical EMT characteristics in cancer cells.
E-cadherin, a typical epithelial cell marker, was markedly decreased in T-synthase knockout HCT 116 cells, accompanied by an enhanced expression of mesenchymal markers including snail and fibronectin (FN).
Conclusions.
These findings indicate that T-synthase deficiency in CRC cells not only is responsible for aberrant O-glycosylation, but also triggers the molecular process of EMT pathway, which may translate to increased invasiveness and metastasis in cancers.
American Psychological Association (APA)
Dong, Xichen& Jiang, Yuliang& Liu, Jian& Liu, Zhe& Gao, Tianbo& An, Guangyu…[et al.]. 2018. T-Synthase Deficiency Enhances Oncogenic Features in Human Colorectal Cancer Cells via Activation of Epithelial-Mesenchymal Transition. BioMed Research International،Vol. 2018, no. 2018, pp.1-7.
https://search.emarefa.net/detail/BIM-1129848
Modern Language Association (MLA)
Dong, Xichen…[et al.]. T-Synthase Deficiency Enhances Oncogenic Features in Human Colorectal Cancer Cells via Activation of Epithelial-Mesenchymal Transition. BioMed Research International No. 2018 (2018), pp.1-7.
https://search.emarefa.net/detail/BIM-1129848
American Medical Association (AMA)
Dong, Xichen& Jiang, Yuliang& Liu, Jian& Liu, Zhe& Gao, Tianbo& An, Guangyu…[et al.]. T-Synthase Deficiency Enhances Oncogenic Features in Human Colorectal Cancer Cells via Activation of Epithelial-Mesenchymal Transition. BioMed Research International. 2018. Vol. 2018, no. 2018, pp.1-7.
https://search.emarefa.net/detail/BIM-1129848
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1129848