Feedback Activation of STAT3 as a Cancer Drug-Resistance Mechanism

详细信息    查看全文

• 作者：Chengguang Zhao¹ ; ² ; ³ ; ⁵ ; Huameng Li³ ; ⁵ ; Huey-Jen Lin⁴ ; Shulin Yang¹ ; ^{bioshuliny@yahoo.com.cn" class="auth_mail" title="E-mail the corresponding author} ; Jiayuh Lin² ; ^{lin.674@osu.edu" class="auth_mail" title="E-mail the corresponding author} ; Guang Liang³
• 关键词：STAT3 ; activation ; inhibitor ; drug-resistance ; cancer
• 刊名：Trends in Pharmacological Sciences
• 出版年：2016
• 出版时间：January 2016
• 年：2016
• 卷：37
• 期：1
• 页码：47-61
• 全文大小：2756 K

文摘

Signal transducer and activator of transcription 3 (STAT3) plays crucial roles in several cellular processes such as cell proliferation and survival, and has been found to be aberrantly activated in many cancers. Much research has explored the leading mechanisms for regulating the STAT3 pathway and its role in promoting tumorigenesis. We focus here on recent evidence suggesting that feedback activation of STAT3 plays a prominent role in mediating drug resistance to a broad spectrum of targeted cancer therapies and chemotherapies. We highlight the potential of co-targeting STAT3 and its primary target to overcome drug resistance, and provide perspective on repurposing clinically approved drugs as STAT3 pathway inhibitors, in combination with the FDA-approved receptor tyrosine kinase (RTK) inhibitors, to improve clinical outcome of cancer treatment.