التفاصيل البيبلوغرافية
| العنوان: |
Aberrant Expression of ADARB1 Facilitates Temozolomide Chemoresistance and Immune Infiltration in Glioblastoma. |
| المؤلفون: |
Lu, Can, Chen, Xi, Yan, Yuanliang, Ren, Xinxin, Wang, Xiang, Peng, Bi, Cai, Yuan, Liang, Qiuju, Xu, Zhijie, Peng, Jinwu |
| المصدر: |
Frontiers in Pharmacology; 2/1/2022, Vol. 13, p1-14, 14p |
| مصطلحات موضوعية: |
RNA editing, TEMOZOLOMIDE, NEUROTRANSMITTER receptors, RNA modification & restriction, DRUG resistance in cancer cells, ADENOSINE deaminase |
| مستخلص: |
Chemoresistance, especially temozolomide (TMZ) resistance, is a major clinical challenge in the treatment of glioblastoma (GBM). Exploring the mechanisms of TMZ resistance could help us identify effective therapies. Adenosine deaminases acting on RNA (ADARs) are very important in RNA modification through regulating the A-to-I RNA editing. Recent studies have shown that ADARs regulate multiple neurotransmitter receptors, which have been linked with the occurrence and progress of GBM. Here, data from several bioinformatics databases demonstrated that adenosine deaminase RNA specific B1 (ADARB1), also named ADAR2, was upregulated in both GBM tissues and cells, and had the prognostic value in GBM patients. Moreover, ADARB1 was found to be involved in AKT-mediated TMZ resistance in GBM cells. The KEGG analysis of ADARB1-associated co-expressed genes showed that ADARB1 was potentially involved in the mitochondrial respiratory chain complex. TISIDB and GEPIA databases were further used to analyze the role of ADARB1 in tumor-immune system interactions in GBM. These findings deepened our understanding of the function of ADARB1 in tumorigenesis and therapeutic response in GBM. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
Complementary Index |
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