TGF-β - an excellent servant but a bad master.
TGF-β - an excellent servant but a bad master.
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DOI：
10.1186/1479-5876-10-183
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发表时间：
2012-09-03
影响因子：
7.4
通讯作者：
Sevcikova S
中科院分区：
文献类型：
--
作者：
Kubiczkova L;Sedlarikova L;Hajek R;Sevcikova S
生长因子的转化生长因子（TGF-β）家族控制大量的细胞反应，并且在大多数人体组织的发育和稳态中占显著地位。过去几十年的工作揭示了对TGF-β信号转导网络的重要见解，例如通过配体结合激活丝氨酸/苏氨酸受体，通过磷酸化激活SMAD蛋白，调节与DNA结合伴侣相关的靶基因表达以及调节SMAD活性和降解。TGF-β通路的破坏与许多人类疾病有关，包括实体瘤和造血系统肿瘤。TGF-β作为一种有效的细胞增殖抑制剂，具有肿瘤抑制作用;但在肿瘤细胞中，TGF-β失去抗增殖反应，成为一种致癌因子。本文综述了目前对TGF-β信号传导的理解以及导致其在各种实体瘤和恶性血液病中受损的不同机制。
The transforming growth factor (TGF-β) family of growth factors controls an immense number of cellular responses and figures prominently in development and homeostasis of most human tissues. Work over the past decades has revealed significant insight into the TGF-β signal transduction network, such as activation of serine/threonine receptors through ligand binding, activation of SMAD proteins through phosphorylation, regulation of target genes expression in association with DNA-binding partners and regulation of SMAD activity and degradation. Disruption of the TGF-β pathway has been implicated in many human diseases, including solid and hematopoietic tumors. As a potent inhibitor of cell proliferation, TGF-β acts as a tumor suppressor; however in tumor cells, TGF-β looses anti-proliferative response and become an oncogenic factor. This article reviews current understanding of TGF-β signaling and different mechanisms that lead to its impairment in various solid tumors and hematological malignancies.
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