摘要
转录因子3(STAT3)的信号转换器和催化剂在许多癌症类型中被激活,且可以调节多种通路包括肿瘤发生、细胞增殖、细胞生存和血管生成。穿过多重转化膜受体的上游细胞因子信号能够增强STAT3的活化作用和促进肿瘤恶化。重要的是,STAT3激活也能够诱导Janus激活的激酶1/2(JAK1/2)和Src家族激酶。靶向药物疗法已经发展了用来抑制许多STAT3的上游受体和非受体活化剂,且现在已经被批准用于临床。最近,对规范化治疗的抵抗与STAT3激活的要素和有增无减联系在一起,表明STAT3抑制剂联合疗法可能具有临床优势。此外,STAT3活性也被证明能够调节癌症干细胞的自我更新,而这通常产生化学疗法的耐药性。这篇综述聚焦于STAT3介导的癌症治疗的耐药性和讨论战胜这种耐药性的策略。
关键词: 癌症治疗,药物抗性,抗辐射性,STAT3,肿瘤耐药性
Current Drug Targets
Title:The Role of STAT3 Signaling in Mediating Tumor Resistance to Cancer Therapy
Volume: 15 Issue: 14
Author(s): Fiona H. Tan, Tracy L. Putoczki, Stanley S. Stylli and Rodney B. Luwor
Affiliation:
关键词: 癌症治疗,药物抗性,抗辐射性,STAT3,肿瘤耐药性
摘要: Signal transducer and activator of transcription 3 (STAT3) is activated in many cancer types and can regulate pathways involving tumorigenesis, cell proliferation, cell survival and angiogenesis. Upstream cytokine signaling through multiple trans-membrane receptors can enhance the activation of STAT3 and promote tumor progression. Importantly, STAT3 activation can also be induced via the Janus-activated kinase 1/2 (JAK1/2) and Src family kinases. Target-specific drug therapies have been developed to inhibit many of the upstream receptor and non-receptor activators of STAT3 and are now approved for clinical use. Recently, resistance to standard-of-care therapies has been linked to constitutive or unabated STAT3 activation, suggesting that combination therapy with STAT3 inhibitors may be of clinical benefit. Furthermore, STAT3 activity has also been shown to regulate self-renewal of cancer stem cells that are often refractory to chemotherapy treatment. This review will focus on STAT3 mediated resistance to cancer therapy and discuss strategies to overcome this resistance.
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Cite this article as:
Fiona H. Tan, Tracy L. Putoczki, Stanley S. Stylli and Rodney B. Luwor , The Role of STAT3 Signaling in Mediating Tumor Resistance to Cancer Therapy, Current Drug Targets 2014; 15 (14) . https://dx.doi.org/10.2174/1389450115666141120104146
DOI https://dx.doi.org/10.2174/1389450115666141120104146 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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