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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Constitutive activation of Stat3 signaling abrogates apoptosis in squamous cell carcinogenesis in vivo
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Constitutive activation of Stat3 signaling abrogates apoptosis in squamous cell carcinogenesis in vivo

机译：Stat3信号传导的本构激活消除了体内鳞状细胞癌的细胞凋亡。

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摘要

Field cancerization predisposes the upper aerodigestive tract mu- cosa to the formation of multiple primary tumors, when exposed to environmental carcinogens. Up-regulation of epidermal growth factor receptor occurs early in squamous cell carcinogenesis and is critical for the loss of growth control in a variety of human cancers, including head and neck squamous cell carcinomas. In these tumor cells in culture. epidermal growth factor receptor stimulation initiates signaling via persistent activation of selective STAT pro- teins. To determine the timing of Stat3 activation in head and neck carcinogenesis, we studied the expression and constitutive activa- tion of Stat3 in tumors and normal mucosa from patients with head and neck cancer compared with mucosa from controls without cancer. Stat3 was up-regulated and constitutively activated in both primary human head and neck tumors as well as in normal mucosa from these cancer patients compared with control normal mucosa from patients without cancer. In vivo liposome-mediated gene therapy with a Stat3 antisense plasmid efficiently inhibited Stat3 activation, increased tumor cell apoptosis, and decreased Bcl-xL expression in a head and neck xenograft model. These findings provide evidence that constitutively activated Stat3 is an early event in head and neck carcinogenesis that contributes to the loss of growth control by an anti-apoptotic mechanism.
机译：当暴露于环境致癌物时，田间癌变使上消化道粘膜易于形成多个原发性肿瘤。表皮生长因子受体的上调发生在鳞状细胞癌变的早期，对于丧失包括头颈部鳞状细胞癌在内的多种人类癌症的生长控制至关重要。在这些肿瘤细胞中进行培养。表皮生长因子受体刺激通过选择性STAT蛋白的持续活化来启动信号传导。为了确定Stat3激活在头颈部癌变中的时机，我们研究了Stat3在头颈部癌患者的肿瘤和正常黏膜中与无癌对照组的黏膜相比的表达和组成性激活。与未患癌症的正常对照相比，这些癌症患者的原发性人头和颈部肿瘤以及正常黏膜中的Stat3被上调并组成性激活。 Stat3反义质粒的体内脂质体介导的基因治疗可有效抑制Stat3激活，增加肿瘤细胞凋亡并降低头颈部异种移植模型中的Bcl-xL表达。这些发现提供了证据，表明组成性激活的Stat3是头颈部癌变的早期事件，其通过抗凋亡机制导致生长控制的丧失。

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