Abstract

Interleukin-33 (IL-33) is a member of the IL-1 cytokine family, primarily known as a mediator of the humoral immune response. It provides protection of barrier tissues and participates in the development of a range of diseases. This cytokine promotes carcinogenesis by induction of proliferation and survival of cancer cells, remodeling of the tumor microenvironment, and promoting immunosuppressive conditions. Elevated levels of IL-33 were observed in many types of cancers. This elevation correlates with a poor prognosis, making IL33 a promising target for cancer immunotherapy. The mechanisms of IL-33 expression regulation in human tumor cells are not well understood. Here, we show that that expression of IL-33 in breast and lung cancer cell lines depends, at least in part, on the activity of the SP1 and FOXA1 transcription factors. Increases in the activity of these transcription factors may be responsible for elevated levels of IL-33 and subsequent tumor progression.

中文翻译：

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SP1和Foxa1对乳腺癌和肺癌细胞IL33基因表达的调控

摘要

白介素33（IL-33）是IL-1细胞因子家族的成员，主要被称为体液免疫反应的介体。它提供屏障组织的保护，并参与多种疾病的发展。该细胞因子通过诱导癌细胞的增殖和存活，肿瘤微环境的重塑以及促进免疫抑制条件来促进癌变。在许多类型的癌症中均观察到IL-33水平升高。这种升高与预后不良相关，使IL33癌症免疫疗法的有希望的靶标。人们对人类肿瘤细胞中IL-33表达调节的机制还不甚了解。在这里，我们表明乳腺癌和肺癌细胞系中IL-33的表达至少部分取决于SP1和FOXA1转录因子的活性。这些转录因子活性的增加可能与IL-33水平升高和随后的肿瘤进展有关。