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
تقوم هذه الخدمة بالتحقق من التشابه أو الانتحال في الأبحاث والمقالات العلمية والأطروحات الجامعية والكتب والأبحاث باللغة العربية، وتحديد درجة التشابه أو أصالة الأعمال البحثية وحماية ملكيتها الفكرية. تعرف اكثر