دورية أكاديمية

The Role of Receptor for Advanced Glycation End Products (RAGE) in the Proliferation of Hepatocellular Carcinoma

التفاصيل البيبلوغرافية
العنوان: The Role of Receptor for Advanced Glycation End Products (RAGE) in the Proliferation of Hepatocellular Carcinoma
المؤلفون: Wei Tian, Dao-Lin Tang, Xue-Gong Fan, Chao-Jun Duan, Zhe-Bing Huang, Mei-Fang Xiao, Guan-Sheng Hu, Al-Madhagi Yaser, Yan Huang, Rong-Rong Zhou
المصدر: International Journal of Molecular Sciences, Vol 13, Iss 5, Pp 5982-5997 (2012)
بيانات النشر: MDPI AG, 2012.
سنة النشر: 2012
المجموعة: LCC:Biology (General)
LCC:Chemistry
مصطلحات موضوعية: RAGE, HMGB1, siRNA, NF-κB, proliferation, Biology (General), QH301-705.5, Chemistry, QD1-999
الوصف: The receptor for advanced glycation end products (RAGE) is oncogenic and overexpressed in human cancers, but its role in hepatocellular carcinoma remains unclear. Here we demonstrated that RAGE is overexpressed in primary hepatocellular carcinoma (PHC) compared to adjacent para-neoplastic liver samples. Serum endogenous secretory RAGE levels were also increased in PHC patients (p < 0.01). Moreover, we demonstrated that RAGE regulates cellular proliferation in Hepatocellular carcinoma (HCC). Knockdown of RAGE by specific siRNA inhibited cellular growth in the hepatocellular carcinoma cell line, Huh7, whereas the RAGE ligand, high mobility group box 1 protein (HMGB1) increased cellular proliferation. In addition, knockdown of RAGE by siRNA arrested cells in the G1 phase and inhibited DNA synthesis (p < 0.01), while HMGB1 protein decreased the number of cells in the G1 phase and increased the number in the S phase (p < 0.05). Furthermore, quantitative real time RT-PCR (qRT-PCR) and Western Blot results demonstrated that RAGE and HMGB1 positively regulate NF-κB p65 expression in Huh7 cells. These studies suggest that RAGE and RAGE ligands are important targets for therapeutic intervention in hepatocellular carcinoma.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1422-0067
Relation: http://www.mdpi.com/1422-0067/13/5/5982; https://doaj.org/toc/1422-0067
DOI: 10.3390/ijms13055982
URL الوصول: https://doaj.org/article/831cb7ff3f3f4a5bb490d50124dd5f94
رقم الأكسشن: edsdoj.831cb7ff3f3f4a5bb490d50124dd5f94
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:14220067
DOI:10.3390/ijms13055982