STAT3, the Challenge for Chemotherapeutic and Radiotherapeutic Efficacy.
STAT3, the Challenge for Chemotherapeutic and Radiotherapeutic Efficacy.
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STAT3，化疗和放疗疗效的挑战
DOI：
10.3390/cancers12092459
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发表时间：
2020-08-30
期刊：
影响因子：
5.2
通讯作者：
Xu LY
中科院分区：
文献类型：
--
作者：
Yang PL;Liu LX;Li EM;Xu LY
STAT3是一种癌基因，导致肿瘤对化疗和放疗的不敏感，降低临床疗效。同时，STAT3β作为一种STAT3剪接异构体，与抑制肿瘤生长和抑制化疗敏感性有关。STAT3可能成为克服化疗(放射)耐药的潜在靶点，这有利于开发针对STAT3或选择性剪接调节因子的新药。放化疗是治疗癌症最有效、应用最广泛的策略之一。信号转导和转录激活子3(STAT3)调控细胞增殖和生长等重要的生物学过程。它在多种癌症中被结构性激活，限制了放化疗的应用。越来越多的证据表明，STAT3通过调节其反馈环和几个靶基因来调节对化疗和放疗的耐药性，从而损害治疗效果。选择性剪接产物STAT3β通常被认为是显性-负性调节因子，但它增强了对化疗的敏感性，并提供了一种新的具有挑战性的方法来逆转治疗耐药。我们在这里重点探讨STAT3在受体酪氨酸激酶(RTK)抑制剂耐药和放射治疗中的作用，概述靶向STAT3克服化疗(放射)耐药以改善临床结果的潜力，并评估STAT3β作为克服化疗(放射)耐药的潜在治疗方法的重要性。在这篇综述中，我们讨论了一些关于STAT3及其亚型β对放化疗敏感性影响的新见解，并探讨了这些见解如何影响癌症的临床治疗和药物开发。
STAT3, an oncogene, contributes to insensitivity of chemotherapy and radiotherapy in tumor, reduces the clinical efficacy. Meanwhile, STAT3β, a STAT3 splicing isoform, is related to the inhibition of tumor growth and chemosensitivity. STAT3 may become a potential target to overcome the chemo(radio)resistance, which benefit for developing novel drugs targeting STAT3 or alternative splicing regulators. Chemoradiotherapy is one of the most effective and extensively used strategies for cancer treatment. Signal transducer and activator of transcription 3 (STAT3) regulates vital biological processes, such as cell proliferation and cell growth. It is constitutively activated in various cancers and limits the application of chemoradiotherapy. Accumulating evidence suggests that STAT3 regulates resistance to chemotherapy and radiotherapy and thereby impairs therapeutic efficacy by mediating its feedback loop and several target genes. The alternative splicing product STAT3β is often identified as a dominant-negative regulator, but it enhances sensitivity to chemotherapy and offers a new and challenging approach to reverse therapeutic resistance. We focus here on exploring the role of STAT3 in resistance to receptor tyrosine kinase (RTK) inhibitors and radiotherapy, outlining the potential of targeting STAT3 to overcome chemo(radio)resistance for improving clinical outcomes, and evaluating the importance of STAT3β as a potential therapeutic approach to overcomes chemo(radio)resistance. In this review, we discuss some new insights into the effect of STAT3 and its subtype STAT3β on chemoradiotherapy sensitivity, and we explore how these insights influence clinical treatment and drug development for cancer.
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