Malla Ritu, Ashby Charles R, Narayanan Narayanan K, Narayanan Bhagavathi, Faridi Jesika S, Tiwari Amit K
Department of Physiology and Pharmacology, Thomas J. Long School of Pharmacy and Health Sciences University of the Pacific, Stockton, CA, USA.
Department of Pharmaceutical Sciences, St. John's University, Queens, NY, USA.
Biochem Biophys Res Commun. 2015 Jul 31;463(3):161-6. doi: 10.1016/j.bbrc.2015.05.041. Epub 2015 May 20.
Dysregulation of PI3K-AKT-mTOR pathway has been reported in various pathologies, such as cancer and insulin resistance. The proline-rich AKT substrate of 40-kDa (PRAS40), also known as AKT substrate 1 (AKT1S1), lies at the crossroads of these cascades and inhibits the activity of the mTOR complex 1 (mTORC1) kinase. This review discusses the role of PRAS40 and possible feedback mechanisms, and alterations in AKT/PRAS40/mTOR signaling that have been implicated in the pathogenesis of tumor progression. Additionally, we probed new datasets extracted from Oncomine, a cancer microarray database containing datasets derived from patient samples, to further understand the role of PRAS40 (AKT1S1). These data strongly supports the hypothesis that PRAS40 may serve as a potential therapeutic target for various cancers.
PI3K-AKT-mTOR信号通路的失调在多种病理状况中都有报道，如癌症和胰岛素抵抗。富含脯氨酸的40 kDa AKT底物（PRAS40），也被称为AKT底物1（AKT1S1），处于这些级联反应的交汇点，并抑制mTOR复合物1（mTORC1）激酶的活性。本综述讨论了PRAS40的作用和可能的反馈机制，以及AKT/PRAS40/mTOR信号传导的改变，这些改变与肿瘤进展的发病机制有关。此外，我们探究了从Oncomine（一个包含来自患者样本数据集的癌症微阵列数据库）中提取的新数据集，以进一步了解PRAS40（AKT1S1）的作用。这些数据有力地支持了PRAS40可能作为各种癌症潜在治疗靶点的假说。
Zotero 插件