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本文引用的文献

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Single nucleotide polymorphism at rs1982073:T869C of the TGFbeta 1 gene is associated with the risk of radiation pneumonitis in patients with non-small-cell lung cancer treated with definitive radiotherapy.转化生长因子β1(TGFβ1)基因rs1982073处的单核苷酸多态性:T869C与接受根治性放疗的非小细胞肺癌患者发生放射性肺炎的风险相关。
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2
Elevation of plasma TGF-beta1 during radiation therapy predicts radiation-induced lung toxicity in patients with non-small-cell lung cancer: a combined analysis from Beijing and Michigan.放射治疗期间血浆转化生长因子-β1升高可预测非小细胞肺癌患者的放射性肺损伤:来自北京和密歇根的联合分析
Int J Radiat Oncol Biol Phys. 2009 Aug 1;74(5):1385-90. doi: 10.1016/j.ijrobp.2008.10.065. Epub 2009 Feb 21.
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SMAD6 contributes to patient survival in non-small cell lung cancer and its knockdown reestablishes TGF-beta homeostasis in lung cancer cells.SMAD6有助于非小细胞肺癌患者的生存,其敲低可重建肺癌细胞中的TGF-β稳态。
Cancer Res. 2008 Dec 1;68(23):9686-92. doi: 10.1158/0008-5472.CAN-08-1083.
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Inhibition of TGF-beta2 with AP 12009 in recurrent malignant gliomas: from preclinical to phase I/II studies.AP 12009对复发性恶性胶质瘤中转化生长因子-β2的抑制作用:从临床前研究到I/II期研究
Oligonucleotides. 2007 Summer;17(2):201-12. doi: 10.1089/oli.2006.0053.
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Stable overexpression of Smad7 in human melanoma cells impairs bone metastasis.Smad7在人黑色素瘤细胞中的稳定过表达会损害骨转移。
Cancer Res. 2007 Mar 1;67(5):2317-24. doi: 10.1158/0008-5472.CAN-06-3950.
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Effect of Smad7 expression on metastasis of mouse mammary carcinoma JygMC(A) cells.Smad7表达对小鼠乳腺癌JygMC(A)细胞转移的影响。
J Natl Cancer Inst. 2005 Dec 7;97(23):1734-46. doi: 10.1093/jnci/dji399.
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Non-Smad TGF-beta signals.非Smad转化生长因子-β信号
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8
Selective inhibitors of type I receptor kinase block cellular transforming growth factor-beta signaling.I型受体激酶的选择性抑制剂可阻断细胞转化生长因子-β信号传导。
Biochem Pharmacol. 2004 Jul 1;68(1):41-50. doi: 10.1016/j.bcp.2004.03.011.
9
SB-505124 is a selective inhibitor of transforming growth factor-beta type I receptors ALK4, ALK5, and ALK7.SB-505124是转化生长因子-β I型受体ALK4、ALK5和ALK7的选择性抑制剂。
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10
Smad7 but not Smad6 cooperates with oncogenic ras to cause malignant conversion in a mouse model for squamous cell carcinoma.在鳞状细胞癌小鼠模型中,Smad7而非Smad6与致癌性Ras协同作用导致恶性转化。
Cancer Res. 2003 Nov 15;63(22):7760-8.

TGF-β 信号转导及抑制性 Smads 在非小细胞肺癌中的作用。

TGF-beta signaling and the role of inhibitory Smads in non-small cell lung cancer.

机构信息

Department of Biochemistry and Cell Biology, School of Medicine, Kyungpook National University, Daegu, Republic of Korea.

出版信息

J Thorac Oncol. 2010 Apr;5(4):417-9. doi: 10.1097/JTO.0b013e3181ce3afd.

DOI:10.1097/JTO.0b013e3181ce3afd
PMID:20107423
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3637970/
Abstract

The signaling pathway mediated by transforming growth factor-beta (TGF-beta) participates in various biologic processes, including cell growth, differentiation, angiogenesis, apoptosis, and extracellular matrix remodeling. In the context of cancer, TGF-beta signaling can inhibit tumor growth in early-stage tumors. However, in late-stage tumors, the very same pathway promotes tumor invasiveness and metastasis. This paradoxical effect is mediated through similar to mothers against decapentaplegic or Smad protein dependent and independent mechanisms and provides an opportunity for targeted cancer therapy. This review summarizes the molecular process of TGF-beta signaling and the changes in inhibitory Smads that contribute to lung cancer progression. We also present current approaches for rational therapies that target the TGF-beta signaling pathway in cancer.

摘要

转化生长因子-β(TGF-β)介导的信号通路参与多种生物学过程,包括细胞生长、分化、血管生成、凋亡和细胞外基质重塑。在癌症的背景下,TGF-β信号通路可以抑制早期肿瘤的生长。然而,在晚期肿瘤中,同样的通路促进肿瘤的侵袭和转移。这种矛盾的效应是通过类似母亲抗 decapentaplegic 或 Smad 蛋白依赖和非依赖的机制介导的,为靶向癌症治疗提供了机会。本文总结了 TGF-β信号通路的分子过程以及抑制性 Smad 蛋白的变化在促进肺癌进展中的作用。我们还介绍了目前针对癌症中 TGF-β信号通路的合理治疗方法。