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Sweet-P对糖皮质激素受体β的抑制作用作为一种潜在的癌症治疗方法。

Sweet-P inhibition of glucocorticoid receptor β as a potential cancer therapy.

作者信息

Nwaneri Assumpta C, McBeth Lucien, Hinds Terry D

机构信息

Center for Hypertension and Personalized Medicine, Department of Physiology & Pharmacology, University of Toledo College of Medicine, Toledo OH 43614, USA.

出版信息

Cancer Cell Microenviron. 2016;3(3). Epub 2016 Jul 5.

Abstract

The need for the development of new cancer therapies and push for the design of new targeting techniques is on the rise, and would be useful for cancers that are resistant to current drug treatments. The understanding of the genome has significantly advanced cancer therapy, as well as prevention and earlier detection. This research highlight discusses a potential new type of cancer-targeting molecule, Sweet-P, which is the first of its kind. Sweet-P specifically targets the microRNA-144 binding site in the 3' untranslated region (3' UTR) of the human glucocorticoid receptor β (GRβ), which has been demonstrated to increase expression. GRβ has been shown to be highly expressed in cells from solid tumors of uroepithelial carcinomas, gliomas, osteosarcomas, and hepatocellular carcinomas, as well as in liquid tumor cells from leukemia patients. In non-cancerous diseases, GRβ has been shown to be highly expressed in glucocorticoid-resistant asthma. These maladies brought the need for the development of the Sweet-P anti-GRβ molecule. Sweet-P was shown to repress the migration of bladder cancer cells, and may serve as a new therapeutic for GRβ-related diseases.

摘要

开发新的癌症治疗方法以及推动新型靶向技术设计的需求不断增加,这对于对当前药物治疗有抗性的癌症将是有用的。对基因组的了解显著推进了癌症治疗以及预防和早期检测。本研究亮点讨论了一种潜在的新型癌症靶向分子Sweet-P,它是同类中的首个分子。Sweet-P特异性靶向人类糖皮质激素受体β(GRβ)3'非翻译区(3'UTR)中的微小RNA-144结合位点,该位点已被证明会增加表达。GRβ已被证明在尿路上皮癌、神经胶质瘤、骨肉瘤和肝细胞癌的实体瘤细胞以及白血病患者的液体肿瘤细胞中高度表达。在非癌性疾病中,GRβ已被证明在糖皮质激素抵抗性哮喘中高度表达。这些疾病促使了Sweet-P抗GRβ分子的开发。Sweet-P被证明可抑制膀胱癌细胞的迁移,并可能成为治疗GRβ相关疾病的新疗法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ace7/4959805/756809876e50/nihms801202f1.jpg

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