The duality of STAT2 mediated type I interferon signaling in the tumor microenvironment and chemoresistance.
The duality of STAT2 mediated type I interferon signaling in the tumor microenvironment and chemoresistance.
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STAT2介导的I型干扰素信号在肿瘤微环境和化疗耐药性中的双重性
DOI：
10.1016/j.cyto.2022.156081
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发表时间：
2023-01
期刊：
影响因子：
3.8
通讯作者：
Gamero, Ana M.
中科院分区：
文献类型：
--
作者：
Canar, Jorge;Darling, Kennedy;Dadey, Ryan;Gamero, Ana M.
肿瘤微环境由肿瘤细胞、细胞外基质、血管以及成纤维细胞和免疫细胞等非肿瘤细胞组成。该细胞生态系统各组成部分之间的串扰可以转化非恶性细胞并促进肿瘤侵袭和转移。越来越多的证据表明，转录因子 STAT2（I 型干扰素 (IFN-I) 信号传导的下游效应子）可以抑制或促进肿瘤发生，具体取决于每种癌症所呈现的独特环境。 STAT2 长期以来一直与参与各种生物过程（包括重塑肿瘤微环境和抗肿瘤免疫）的经典 JAK/STAT 通路相关。 STAT2 抑制和恶化肿瘤形成的这种二分倾向使得该蛋白在许多涉及 IFN-I 的癌症通路中成为一个令人好奇但相对不明确的参与者。在这篇综述中，我们讨论了 STAT2 在致瘤或抗肿瘤微环境以及化疗耐药中的作用。
The tumor microenvironment consists of tumor cells, extracellular matrix, blood vessels, and non-tumor cells such as fibroblasts and immune cells. Crosstalk among components of this cellular ecosystem can transform non-malignant cells and promote tumor invasion and metastasis. Evidence is accumulating that the transcription factor STAT2, a downstream effector of type I interferon (IFN-I) signaling, can either inhibit or promote tumorigenesis depending on the unique environment presented by each type of cancer. STAT2 has long been associated with the canonical JAK/STAT pathway involved in various biological processes including reshaping of the tumor microenvironment and in antitumor immunity. This dichotomous tendency of STAT2 to both inhibit and worsen tumor formation makes the protein a curious, and yet relatively ill-defined player in many cancer pathways involving IFN-I. In this review, we discuss the role of STAT2 in contributing to either a tumorigenic or anti-tumorigenic microenvironment as well as chemoresistance.
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影响因子：
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DOI：
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期刊：
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