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YDJC Induces Epithelial-Mesenchymal Transition via Escaping from Interaction with CDC16 through Ubiquitination of PP2A
المؤلفون المشاركون
Kim, Eun Ji
Park, Mi Kyung
Kang, Gyeoung-Jin
Byun, Hyun Jung
Kim, Hyun Ji
Yu, Lu
Kim, Boram
Chae, Hee-Sung
Chin, Young-Won
Shim, Jae Gal
Lee, Ho
Lee, Chang Hoon
المصدر
العدد
المجلد 2019، العدد 2019 (31 ديسمبر/كانون الأول 2019)، ص ص. 1-15، 15ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2019-08-07
دولة النشر
مصر
عدد الصفحات
15
التخصصات الرئيسية
الملخص EN
Lung cancer is the number 1 cause of cancer-related casualties in the world.
Appropriate diagnostic markers and novel targets for lung cancer are needed.
Chitooligosaccharide deacetylase homolog (YDJC) catalyzes the deacetylation of acetylated carbohydrates; however, the role of YDJC in lung cancer progression has yet to be studied.
A549 lung cancer orthotopic mouse model was used for mice experiments.
We found that YDJC overexpression contributes to lung cancer progression in an orthotopic mouse model.
Long-term treatment (48 h) induces YDJC expression in sphingosylphosphorylcholine (SPC)-induced epithelial-mesenchymal transition (EMT).
Gene silencing of YDJC (siYDJC) reduced N-cadherin expression and increased E-cadherin expression in SPC-induced EMT.
Overexpression of YDJC reverses them but overexpression of the deacetylase deficient mutant YDJCD13A could not.
Interestingly, overexpression of CDC16, a YDJC binding partner, suppressed EMT.
ERK2 is activated in siCDC16-induced EMT.
YDJC overexpression reduces expression of protein phosphatase 2A (PP2A), whereas CDC16 overexpression induces PP2A expression.
YDJC overexpression induced ubiquitination of PP2A but YDJCD13A could not.
CDC16 overexpression increased the ubiquitination of YDJC.
These results suggest that YDJC contributes to the progression of lung cancer via enhancing EMT by inducing the ubiquitination of PP2A.
Therefore, YDJC might be a new target for antitumor therapy against lung cancer.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Kim, Eun Ji& Park, Mi Kyung& Kang, Gyeoung-Jin& Byun, Hyun Jung& Kim, Hyun Ji& Yu, Lu…[et al.]. 2019. YDJC Induces Epithelial-Mesenchymal Transition via Escaping from Interaction with CDC16 through Ubiquitination of PP2A. Journal of Oncology،Vol. 2019, no. 2019, pp.1-15.
https://search.emarefa.net/detail/BIM-1184151
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Kim, Eun Ji…[et al.]. YDJC Induces Epithelial-Mesenchymal Transition via Escaping from Interaction with CDC16 through Ubiquitination of PP2A. Journal of Oncology No. 2019 (2019), pp.1-15.
https://search.emarefa.net/detail/BIM-1184151
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Kim, Eun Ji& Park, Mi Kyung& Kang, Gyeoung-Jin& Byun, Hyun Jung& Kim, Hyun Ji& Yu, Lu…[et al.]. YDJC Induces Epithelial-Mesenchymal Transition via Escaping from Interaction with CDC16 through Ubiquitination of PP2A. Journal of Oncology. 2019. Vol. 2019, no. 2019, pp.1-15.
https://search.emarefa.net/detail/BIM-1184151
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1184151
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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