Casein Kinase 2 Interacting Protein-1 Suppresses Glioma Cell Proliferation via Regulating the AKTGSK3 β β -Catenin Pathway
المؤلفون المشاركون
Xi, Yan-Guo
Ren, Deng-Peng
Jin, Jing-Yun
Zhu, Lei
Yi, Tai-Long
Shao, Xue-Fei
Sun, Sheng-Kai
Zhang, Wen-Bin
Cheng, Shi-Xiang
المصدر
العدد
المجلد 2019، العدد 2019 (31 ديسمبر/كانون الأول 2019)، ص ص. 1-11، 11ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2019-07-02
دولة النشر
مصر
عدد الصفحات
11
التخصصات الرئيسية
الملخص EN
Objective.
Casein kinase 2 interacting protein-1 (CKIP-1) has exhibited multiple functions in regulating cell proliferation, apoptosis, differentiation, and cytoskeleton.
CKIP-1 also plays an important role as a critical regulator in tumorigenesis.
The aim of this study is to further examine the function of CKIP-1 in glioma cells.
Methods.
The expression level of CKIP-1 protein was determined in gliomas tissues and cell lines by immunohistochemistry stain and western blotting while the association of CKIP-1 expression with prognosis was analyzed by Kaplan-Meier method and compared by log-rank test.
CKIP-1 was overexpressed or silenced in gliomas cell lines.
CCK-8, colony formation assay, and BrdU incorporation assay were used to determine cell proliferation and DNA synthesis.
Cell cycle and apoptosis rate were determined with fluorescence-activated cell sorting (FACS) method.
Then, expression of key members in AKT/GSK3β/β-catenin pathway was detected by western blot analysis.
Results.
In the present study, we reported new evidence that CKIP-1 was reversely associated with the proliferation of glioma cells and survival in glioma patients.
Additionally, the overexpressed CKIP-1 significantly inhibited glioma cell proliferation.
Further experiments revealed that CKIP-1 functioned through its antiproliferative and proapoptotic activity in glioma cells.
Importantly, mechanistic investigations suggested that CKIP-1 sharply suppressed the activity of AKT by inhibiting the phosphorylation, markedly downregulated the phosphorylated GSK3β at Ser9, and promoted β-catenin degradation.
Conclusions.
Overall, our results provided new insights into the clinical significance and molecular mechanism of CKIP-1 in glioma, which indicated CKIP1 might function as a therapeutic target for clinical treatment of glioma.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Xi, Yan-Guo& Ren, Deng-Peng& Jin, Jing-Yun& Zhu, Lei& Yi, Tai-Long& Shao, Xue-Fei…[et al.]. 2019. Casein Kinase 2 Interacting Protein-1 Suppresses Glioma Cell Proliferation via Regulating the AKTGSK3 β β -Catenin Pathway. BioMed Research International،Vol. 2019, no. 2019, pp.1-11.
https://search.emarefa.net/detail/BIM-1126136
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Xi, Yan-Guo…[et al.]. Casein Kinase 2 Interacting Protein-1 Suppresses Glioma Cell Proliferation via Regulating the AKTGSK3 β β -Catenin Pathway. BioMed Research International No. 2019 (2019), pp.1-11.
https://search.emarefa.net/detail/BIM-1126136
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Xi, Yan-Guo& Ren, Deng-Peng& Jin, Jing-Yun& Zhu, Lei& Yi, Tai-Long& Shao, Xue-Fei…[et al.]. Casein Kinase 2 Interacting Protein-1 Suppresses Glioma Cell Proliferation via Regulating the AKTGSK3 β β -Catenin Pathway. BioMed Research International. 2019. Vol. 2019, no. 2019, pp.1-11.
https://search.emarefa.net/detail/BIM-1126136
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1126136
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