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本文引用的文献

1
From keratinocyte to cancer: the pathogenesis and modeling of cutaneous squamous cell carcinoma.从角质形成细胞到癌症：皮肤鳞状细胞癌的发病机制和建模。
J Clin Invest. 2012 Feb;122(2):464-72. doi: 10.1172/JCI57415. Epub 2012 Feb 1.
2
Notch activation by the metalloproteinase ADAM17 regulates myeloproliferation and atopic barrier immunity by suppressing epithelial cytokine synthesis.金属蛋白酶 ADAM17 的 Notch 激活通过抑制上皮细胞细胞因子合成来调节骨髓增生和特应性屏障免疫。
Immunity. 2012 Jan 27;36(1):105-19. doi: 10.1016/j.immuni.2012.01.005.
3
iRhom2 regulation of TACE controls TNF-mediated protection against Listeria and responses to LPS.iRhom2 通过调控 TACE 控制 TNF 介导的李斯特菌保护和 LPS 反应。
Science. 2012 Jan 13;335(6065):229-32. doi: 10.1126/science.1214448.
4
Tumor necrosis factor signaling requires iRhom2 to promote trafficking and activation of TACE.肿瘤坏死因子信号转导需要 iRhom2 促进 TACE 的运输和激活。
Science. 2012 Jan 13;335(6065):225-8. doi: 10.1126/science.1214400.
5
ADAM17: a molecular switch to control inflammation and tissue regeneration.ADAM17：控制炎症和组织再生的分子开关。
Trends Immunol. 2011 Aug;32(8):380-7. doi: 10.1016/j.it.2011.05.005. Epub 2011 Jul 13.
6
Migration of growth factor-stimulated epithelial and endothelial cells depends on EGFR transactivation by ADAM17.生长因子刺激的上皮细胞和内皮细胞的迁移依赖于 ADAM17 对 EGFR 的转激活作用。
Nat Commun. 2011;2:229. doi: 10.1038/ncomms1232.
7
The disintegrin/metalloproteinase Adam10 is essential for epidermal integrity and Notch-mediated signaling.去整合素/金属蛋白酶 Adam10 对于表皮完整性和 Notch 介导的信号转导是必需的。
Development. 2011 Feb;138(3):495-505. doi: 10.1242/dev.055210.
8
The "A Disintegrin And Metalloproteases" ADAM10 and ADAM17: novel drug targets with therapeutic potential?“解整合素和金属蛋白酶”ADAM10 和 ADAM17：具有治疗潜力的新型药物靶点？
Eur J Cell Biol. 2011 Jun-Jul;90(6-7):527-35. doi: 10.1016/j.ejcb.2010.11.005. Epub 2010 Dec 30.
9
Functions of Fos phosphorylation in bone homeostasis, cytokine response and tumourigenesis.成纤维细胞生长因子受体底物 14 在骨稳态、细胞因子反应和肿瘤发生中的功能
Oncogene. 2011 Mar 31;30(13):1506-17. doi: 10.1038/onc.2010.542. Epub 2010 Nov 29.
10
Stage-specific sensitivity to p53 restoration during lung cancer progression.肺癌进展过程中对 p53 恢复的阶段特异性敏感性。
Nature. 2010 Nov 25;468(7323):572-5. doi: 10.1038/nature09535.

诱导分化抑制皮肤癌的 FOS、p53 和 TACE/ADAM17。

Differentiation-induced skin cancer suppression by FOS, p53, and TACE/ADAM17.

机构信息

Fundación Banco Bilbao Vizcaya (F-BBVA) - CNIO Cancer Cell Biology Program, Centro Nacional de Investigaciones Oncológicas (CNIO), Madrid, Spain.

出版信息

J Clin Invest. 2012 Aug;122(8):2898-910. doi: 10.1172/JCI63103. Epub 2012 Jul 9.

DOI:10.1172/JCI63103
PMID:22772468
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3408745/
Abstract

Squamous cell carcinomas (SCCs) are heterogeneous and aggressive skin tumors for which innovative, targeted therapies are needed. Here, we identify a p53/TACE pathway that is negatively regulated by FOS and show that the FOS/p53/TACE axis suppresses SCC by inducing differentiation. We found that epidermal Fos deletion in mouse tumor models or pharmacological FOS/AP-1 inhibition in human SCC cell lines induced p53 expression. Epidermal cell differentiation and skin tumor suppression were caused by a p53-dependent transcriptional activation of the metalloprotease TACE/ADAM17 (TNF-α-converting enzyme), a previously unknown p53 target gene that was required for NOTCH1 activation. Although half of cutaneous human SCCs display p53-inactivating mutations, restoring p53/TACE activity in mouse and human skin SCCs induced tumor cell differentiation independently of the p53 status. We propose FOS/AP-1 inhibition or p53/TACE reactivating strategies as differentiation-inducing therapies for SCCs.

摘要

鳞状细胞癌（SCC）是一种具有异质性和侵袭性的皮肤肿瘤，需要创新的靶向治疗。在这里，我们确定了一个受 FOS 负调控的 p53/TACE 通路，并表明 FOS/p53/TACE 轴通过诱导分化来抑制 SCC。我们发现，在小鼠肿瘤模型中敲除表皮 Fos 或在人 SCC 细胞系中使用药理学方法抑制 FOS/AP-1，可诱导 p53 表达。表皮细胞分化和皮肤肿瘤抑制是由 p53 依赖性转录激活金属蛋白酶 TACE/ADAM17（TNF-α转换酶）引起的，这是一个先前未知的 p53 靶基因，它是 NOTCH1 激活所必需的。尽管一半的皮肤 SCC 存在 p53 失活突变，但在小鼠和人皮肤 SCC 中恢复 p53/TACE 活性可独立于 p53 状态诱导肿瘤细胞分化。我们提出了 FOS/AP-1 抑制或 p53/TACE 再激活策略作为 SCC 的诱导分化治疗方法。