LncRNA MALAT1 Regulates miR-144-3p to Facilitate Epithelial-Mesenchymal Transition of Lens Epithelial Cells via the ROSNRF2Notch1Snail Pathway
المؤلفون المشاركون
Ye, Wei
Ma, Jiyuan
Wang, Fang
Wu, Tong
He, Mengmei
Li, Ji
Pei, Rui
Zhang, Luning
Wang, Yafen
Zhou, Jian
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2020، العدد 2020 (31 ديسمبر/كانون الأول 2020)، ص ص. 1-23، 23ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2020-11-16
دولة النشر
مصر
عدد الصفحات
23
التخصصات الرئيسية
الملخص EN
Diabetic cataract is a common complication of diabetes.
The epithelial-mesenchymal transition (EMT) of lens epithelial cells (LECs) is a key event in the development of diabetic cataracts.
Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been reported to be highly expressed in different tissues of diabetic patients.
This study is aimed at investigating the function and mechanism of MALAT1 in the regulation of EMT in human LECs under high glucose conditions.
MALAT1, α-smooth muscle actin (α-SMA), fibronectin (FN), and nuclear factor erythroid-derived 2-like 2 (NRF2) were highly expressed in the LECs of diabetic cataract patients and in the human LECs under high glucose conditions; meanwhile, the decreased expressions of E-cadherin and zonula occludens 1 (ZO-1) were detected.
Knockdown of MALAT1 could significantly reduce ROS, prevent EMT, arrest S phase cell cycle, and suppress the expression of total NRF2 and its nucleus translocation in LECs.
Furthermore, after NRF2 was knocked down, total NRF2, α-SMA, and FN in cells, and NRF2, Notch intracellular domain (NICD), and Snail were decreased in the nucleus.
Using bioinformatics methods, we predicted that MALAT1 and NRF2 shared the same microRNA-144-3p (miR-144-3p) combining site.
Luciferase reporter coupled with qRT-PCR assays revealed that miR-144-3p was a target of MALAT1, which was confirmed to downregulate miR-144-3p in the LECs.
In addition, after transfection of miR-144-3p mimics or inhibitor, western blot assay demonstrated that miR-144-3p negatively regulated the expression of total NRF2, α-SMA, and FN in cells, and NRF2, NICD, and Snail in the nucleus without affecting Kelch-like ECH-associated protein 1 (KEAP1).
Finally, we confirmed that transfection of shMALAT1 inhibited NRF2 expression, and its mediated EMT could be rescued by miR-144-3p inhibitor; transfection of pcDNA3.1-MALAT1 promoted NRF2 expression, and its mediated EMT could be reversed by miR-144-3p inhibitor.
In summary, we demonstrate that MALAT1 regulates miR-144-3p to facilitate EMT of LECs via the ROS/NRF2/Notch1/Snail pathway.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Ye, Wei& Ma, Jiyuan& Wang, Fang& Wu, Tong& He, Mengmei& Li, Ji…[et al.]. 2020. LncRNA MALAT1 Regulates miR-144-3p to Facilitate Epithelial-Mesenchymal Transition of Lens Epithelial Cells via the ROSNRF2Notch1Snail Pathway. Oxidative Medicine and Cellular Longevity،Vol. 2020, no. 2020, pp.1-23.
https://search.emarefa.net/detail/BIM-1205535
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Ye, Wei…[et al.]. LncRNA MALAT1 Regulates miR-144-3p to Facilitate Epithelial-Mesenchymal Transition of Lens Epithelial Cells via the ROSNRF2Notch1Snail Pathway. Oxidative Medicine and Cellular Longevity No. 2020 (2020), pp.1-23.
https://search.emarefa.net/detail/BIM-1205535
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Ye, Wei& Ma, Jiyuan& Wang, Fang& Wu, Tong& He, Mengmei& Li, Ji…[et al.]. LncRNA MALAT1 Regulates miR-144-3p to Facilitate Epithelial-Mesenchymal Transition of Lens Epithelial Cells via the ROSNRF2Notch1Snail Pathway. Oxidative Medicine and Cellular Longevity. 2020. Vol. 2020, no. 2020, pp.1-23.
https://search.emarefa.net/detail/BIM-1205535
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1205535
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