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T-Synthase Deficiency Enhances Oncogenic Features in Human Colorectal Cancer Cells via Activation of Epithelial-Mesenchymal Transition
المؤلفون المشاركون
Wen, Tao
An, Guangyu
Gao, Tianbo
Liu, Jian
Dong, Xichen
Jiang, Yuliang
Liu, Zhe
المصدر
العدد
المجلد 2018، العدد 2018 (31 ديسمبر/كانون الأول 2018)، ص ص. 1-7، 7ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2018-06-21
دولة النشر
مصر
عدد الصفحات
7
التخصصات الرئيسية
الملخص 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.
نمط استشهاد جمعية علماء النفس الأمريكية (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
نمط استشهاد الجمعية الأمريكية للغات الحديثة (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
نمط استشهاد الجمعية الطبية الأمريكية (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
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1129848
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
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