JunB contributes to Id2 repression and the epithelial-mesenchymal transition in response to transforming growth factor-β.
JunB contributes to Id2 repression and the epithelial-mesenchymal transition in response to transforming growth factor-β.
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DOI：
10.1083/jcb.201109045
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发表时间：
2012-03-05
期刊：
影响因子：
--
通讯作者：
Bakin AV
中科院分区：
文献类型：
--
作者：
Gervasi M;Bianchi-Smiraglia A;Cummings M;Zheng Q;Wang D;Liu S;Bakin AV
JunB有助于启动响应TGF-β的上皮-间充质转化和组织纤维化所必需的转录程序。响应于转化生长因子-β（TGF-β）的上皮-间充质转化（EMT）过程通过尚未完全理解的机制促成组织纤维化、伤口愈合和癌症。本研究确定了JunB在EMT和对TGF-β的促纤维化反应中的关键作用。通过小干扰核糖核酸消除JunB消除TGF-β诱导的细胞-细胞连接的破坏、肌动蛋白纤维的形成、粘着斑和纤维化蛋白的表达。JunB通过与转录抑制因子激活转录因子3的相互作用，促进Smad介导的分化抑制因子2的抑制。重要的是，JunB介导促纤维化反应因子、纤连蛋白、纤蛋白-2、原肌球蛋白（Tpm 1）和整合素-β3的TGF-β诱导，这些因子在基质沉积、细胞-基质粘附和肌动蛋白应力纤维中起关键作用。总之，JunB在设定EMT的转录程序和对TGF-β的促纤维化反应中提供了重要的输入。因此，JunB代表了与EMT相关的疾病（包括癌症和纤维化）的重要靶标。
JunB helps set in motion the transcriptional program necessary for the epithelial–mesenchymal transition and tissue fibrosis in response to TGF-β. The process of epithelial–mesenchymal transition (EMT) in response to transforming growth factor–β (TGF-β) contributes to tissue fibrosis, wound healing, and cancer via a mechanism that is not fully understood. This study identifies a critical role of JunB in the EMT and profibrotic responses to TGF-β. Depletion of JunB by small interfering ribonucleic acid abrogates TGF-β–induced disruption of cell–cell junctions, formation of actin fibers, focal adhesions, and expression of fibrotic proteins. JunB contributes to Smad-mediated repression of inhibitor of differentiation 2 through interaction with transcription repressor activating transcription factor 3. Importantly, JunB mediates the TGF-β induction of profibrotic response factors, fibronectin, fibulin-2, tropomyosin (Tpm1), and integrin-β3, which play critical roles in matrix deposition, cell–matrix adhesion, and actin stress fibers. In summary, JunB provides important input in setting the transcriptional program of the EMT and profibrotic responses to TGF-β. Thus, JunB represents an important target in diseases associated with EMT, including cancer and fibrosis.
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影响因子：
11.2
作者：
Deckers, M;van Dinther, M;ten Dijke, P
通讯作者：
ten Dijke, P
影响因子：
7.4
作者：
Bakin, AV;Stourman, NV;Freeman, ML
通讯作者：
Freeman, ML
影响因子：
4.8
作者：
Jayaraman, L;Massagué, J
通讯作者：
Massagué, J
DOI：
10.1083/jcb.132.6.1115
发表时间：
1996-03
期刊：
The Journal of cell biology
影响因子：
--
作者：
Fialka I;Schwarz H;Reichmann E;Oft M;Busslinger M;Beug H
通讯作者：
Beug H
影响因子：
7.5
作者：
Kadler KE;Hill A;Canty-Laird EG
通讯作者：
Canty-Laird EG