了解AKT介导的化学耐药:离子通道与AKT激活之间的关系

Rédoane Daoudi
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引用次数: 0

摘要

克服化疗耐药对顺铂等多种化疗药物来说是一个挑战。ABC转运蛋白如MDR1或MRPs和PI3K/ akt通路已被认为是几种癌症化疗耐药的参与者。在这篇综述中,我们描述了Akt的两个下游靶点:c-myc和p53在化疗耐药中的作用。我们认为p53、c-myc和ABCtransporters表达之间存在潜在联系。因此,Akt和abctransporter介导的化疗耐药之间可能存在联系。最后,我们发现akt激活可能依赖于orai和/或trpc,这表明这些离子通道可能构成癌症的治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Understanding AKT-mediated chemoresistance: the relationship between ion channels and AKT activation
Overcoming chemoresistance is a challenge for multiple chemotherapeutics agents like cisplatin. ABC transporters such as MDR1 or MRPs and PI3K/AKT pathway have been proposed as actors of chemoresistance in several cancers. In this review we describe two downstream targets of Akt: c-myc and p53 in the chemoresistance. We suggest a potential link between p53, c-myc and ABC transporters expression. Consequently a link between Akt and ABC transporters-mediated chemoresistance may exist. Finally we show that Akt activation may be Orai-dependent and/or TRPC-dependent, suggesting that these ion channels could constitute a therapeutic target in cancer.
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