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IκB激酶α通过非依赖NF-κB的途径在上皮源性肿瘤中发挥肿瘤抑制作用(综述)。

IκB kinase α functions as a tumor suppressor in epithelial-derived tumors through an NF-κB-independent pathway (Review).

作者信息

Xie Yuxin, Xie Keqi, Gou Qiheng, Chen Nianyong

机构信息

Department of Radiation Oncology, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. China.

Department of Anesthesiology, Mianyang Central Hospital, Mianyang, Sichuan 621000, P.R. China.

出版信息

Oncol Rep. 2015 Nov;34(5):2225-32. doi: 10.3892/or.2015.4229. Epub 2015 Aug 26.

DOI:10.3892/or.2015.4229
PMID:26323241
Abstract

Recent studies have shown that IκB kinase α (IKKα) plays an important role in human skin cancer and acts as a major regulator for keratinocyte terminal differentiation and proliferation. IKKα deficiency or mutation is associated with human tumor development; thus, overexpression of IKKα could prevent tumor progression. However, findings suggest that IKKα is equally essential for many other epithelial-derived tumors. In the present study, we discussed the role of IKKα as a tumor suppressor in IKKα-mediated epithelial‑derived tumors and its activation pathway, which is different from the traditional NF-κB pathway. The present study provides theoretical basis for understanding the molecular mechanisms involved in IKKα-related tumors.

摘要

最近的研究表明,IκB激酶α(IKKα)在人类皮肤癌中起重要作用,并且是角质形成细胞终末分化和增殖的主要调节因子。IKKα缺乏或突变与人类肿瘤发生有关;因此,IKKα的过表达可以阻止肿瘤进展。然而,研究结果表明,IKKα对许多其他上皮来源的肿瘤同样至关重要。在本研究中,我们探讨了IKKα作为肿瘤抑制因子在IKKα介导的上皮来源肿瘤中的作用及其激活途径,该途径不同于传统的NF-κB途径。本研究为理解IKKα相关肿瘤的分子机制提供了理论依据。

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