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Intracellular and extracellular TGF-β signaling in cancer: some recent topics
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《医学前沿(英文)》 2018年 第12卷 第4期 页码 387-411 doi: 10.1007/s11684-018-0646-8
Transforming growth factor (TGF)-β regulates a wide variety of cellular responses, including cell growth arrest, apoptosis, cell differentiation, motility, invasion, extracellular matrix production, tissue fibrosis, angiogenesis, and immune function. Although tumor-suppressive roles of TGF-β have been extensively studied and well-characterized in many cancers, especially at early stages, accumulating evidence has revealed the critical roles of TGF-β as a pro-tumorigenic factor in various types of cancer. This review will focus on recent findings regarding epithelial-mesenchymal transition (EMT) induced by TGF-β, in relation to crosstalk with some other signaling pathways, and the roles of TGF-β in lung and pancreatic cancers, in which TGF-β has been shown to be involved in cancer progression. Recent findings also strongly suggested that targeting TGF-β signaling using specific inhibitors may be useful for the treatment of some cancers. TGF-β plays a pivotal role in the differentiation and function of regulatory T cells (Tregs). TGF-β is produced as latent high molecular weight complexes, and the latent TGF-β complex expressed on the surface of Tregs contains glycoprotein A repetitions predominant (GARP, also known as leucine-rich repeat containing 32 or LRRC32). Inhibition of the TGF-β activities through regulation of the latent TGF-β complex activation will be discussed.
关键词: TGF-β EMT lung cancer pancreatic cancer latent form immune function GARP
《医学前沿(英文)》 doi: 10.1007/s11684-023-1010-1
关键词: exosomes induce activation impair function CD19 exosomal CD19 antigen
Zfyve16 regulates the proliferation of B-lymphoid cells
Xuemei Zhao, Donghe Li, Qingsong Qiu, Bo Jiao, Ruihong Zhang, Ping Liu, Ruibao Ren
《医学前沿(英文)》 2018年 第12卷 第5期 页码 559-565 doi: 10.1007/s11684-017-0562-3
Zfyve16 (a.k.a. endofin or endosome-associated FYVE-domain protein), a member of the FYVE-domain protein family, is involved in endosomal trafficking and in TGF-β, BMP, and EGFR signaling. The FYVE protein SARA regulates the TGF-β signaling pathway by recruiting Smad2/3 and accelerating their phosphorylation, thereby altering their susceptibility to TGF-β-mediated T cell suppression. Zfyve16 binds to Smad4 and their binding affects the formation of Smad2/3-Smad4 complex in TGF-β signaling. However, the in vivo function of Zfyve16 remains unknown. In this study, we generated a Zfyve16 knockout mouse strain (Zfyve16KO) and examined its hematopoietic phenotypes and hematopoietic reconstruction ability. The proportion of T cells in the peripheral blood of Zfyve16KO mice increases compared with that in wild-type mice. This finding is consistent with the role of Zfyve16 in facilitating TGF-β signaling. Unpredictably, B cell proliferation is inhibited in Zfyve16KO mice. The proliferation potential of Zfyve16KO B-lymphoid cells also significantly decreases in vitro. These results suggest that Zfyve16 inhibits the proliferation of T cells, possibly through the TGF-β signaling, but upregulates the proliferation of B-lymphoid cells.
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《医学前沿(英文)》 2014年 第8卷 第4期 页码 445-455 doi: 10.1007/s11684-014-0378-3
Recent evidences suggested that cyclic guanosine monophosphate-specific phosphodiesterase 5 (PDE5) inhibitor represents an important therapeutic target for cardiovascular diseases. Whether and how it ameliorates cardiac fibrosis, a major cause of diastolic dysfunction and heart failure, is unknown. The purpose of this study was to investigate the effects of PDE5 inhibitor on cardiac fibrosis. We assessed cardiac fibrosis and pathology in mice subjected to transverse aortic constriction (TAC). Oral sildenafil, a PDE5 inhibitor, was administered in the therapy group. In control mice, 4 weeks of TAC induced significant cardiac dysfunction, cardiac fibrosis, and cardiac fibroblast activation (proliferation and transformation to myofibroblasts). Sildenafil treatment markedly prevented TAC-induced cardiac dysfunction, cardiac fibrosis and cardiac fibroblast activation but did not block TAC-induced transforming growth factor-β1 (TGF-β1) production and phosphorylation of Smad2/3. In isolated cardiac fibroblasts, sildenafil blocked TGF-β1-induced cardiac fibroblast transformation, proliferation and collagen synthesis. Furthermore, we found that sildenafil induced phosphorylated cAMP response element binding protein (CREB) and reduced CREB-binding protein 1 (CBP1) recruitment to Smad transcriptional complexes. PDE5 inhibition prevents cardiac fibrosis by reducing CBP1 recruitment to Smad transcriptional complexes through CREB activation in cardiac fibroblasts.
关键词: PDE5 cardiac fibrosis TGF-β CREB
Paeoniflorin prevents hepatic fibrosis of by inhibiting TGF-β1 production from macrophages in mice
CHU Deyong, LI Conglei, SHEN Jilong, WU Qiang
《医学前沿(英文)》 2008年 第2卷 第2期 页码 154-165 doi: 10.1007/s11684-008-0029-7
Genome-wide search for candidate genes determining vertebrae number in pigs
Longchao ZHANG, Jingwei YUE, Xin LIU, Jing LIANG, Kebin ZHAO, Hua YAN, Na LI, Lei PU, Yuebo ZHANG, Huibi SHI, Ligang WANG, Lixian WANG
《农业科学与工程前沿(英文)》 2017年 第4卷 第3期 页码 327-334 doi: 10.15302/J-FASE-2017163
关键词: genome-wide association study number of vertebrae pig SSC7 TGFβ3
标题 作者 时间 类型 操作
initial activation by exosomal CD19 antigen but impair the function of CD19-specific CAR T-cells via TGF-β
期刊论文
Zfyve16 regulates the proliferation of B-lymphoid cells
Xuemei Zhao, Donghe Li, Qingsong Qiu, Bo Jiao, Ruihong Zhang, Ping Liu, Ruibao Ren
期刊论文
Chronic inhibition of cyclic guanosine monophosphate-specific phosphodiesterase 5 prevented cardiac fibrosis through inhibition of transforming growth factor β-induced Smad signaling
null
期刊论文
Paeoniflorin prevents hepatic fibrosis of by inhibiting TGF-β1 production from macrophages in mice
CHU Deyong, LI Conglei, SHEN Jilong, WU Qiang
期刊论文