共查询到20条相似文献,搜索用时 15 毫秒
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Antithetical NFATc1–Sox2 and p53–miR200 signaling networks govern pancreatic cancer cell plasticity 下载免费PDF全文
Shiv K Singh Nai‐Ming Chen Elisabeth Hessmann Jens Siveke Marlen Lahmann Garima Singh Nadine Voelker Sophia Vogt Irene Esposito Ansgar Schmidt Cornelia Brendel Thorsten Stiewe Jochen Gaedcke Howard C Crawford William R Bamlet Jin‐San Zhang Xiao‐Kun Li Thomas C Smyrk Daniel D Billadeau Matthias Hebrok Albrecht Neesse Volker Ellenrieder 《The EMBO journal》2015,34(4):517-530
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Novel blocker of NFAT activation inhibits IL-6 production in human myometrial arteries and reduces vascular smooth muscle cell proliferation 总被引:1,自引:0,他引:1
Nilsson LM Sun ZW Nilsson J Nordström I Chen YW Molkentin JD Wide-Swensson D Hellstrand P Lydrup ML Gomez MF 《American journal of physiology. Cell physiology》2007,292(3):C1167-C1178
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《Cell cycle (Georgetown, Tex.)》2013,12(20):2310-2313
Post-translational modification by SUMO is a dynamic and reversible process and several SUMO-specific proteases that remove SUMO from substrates have been identified. We have recently described the activities of a new SUMO-specific protease, SENP5. We found that SENP5 discriminates between SUMO-1 and SUMO-2/3 and cells depleted of SENP5 by RNAi failed to proliferate. Our findings support the idea that differential substrate selection by the mammalian SUMO-specific proteases underlies their regulation of distinct biological processes. Furthermore, our finding of a non-redundant function for SENP5 in cell proliferation provides further support for the model that, analogous to phosphorylation, cycles of SUMOylation and deSUMOylation regulate orderly progression through cell division. 相似文献
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Matthew C. Stout Shilpa Narayan Emily S. Pillet Joseph M. Salvino Paul M. Campbell 《Biochemical and biophysical research communications》2018,495(3):2264-2269
Increased expression of the chemokine CX3CL1 and its sole receptor, CX3CR1 have been correlated with poor pancreatic cancer patient survival and time to recurrence, as well as with pancreatic perineural invasion. We have previously shown that metastasis of prostate and breast cancer is in part driven by CX3CL1, and have developed small molecule inhibitors against the CX3CR1 receptor that diminish metastatic burden. Here we ask if inhibition of this chemokine receptor affects the phenotype of PDAC tumor cells. Our findings demonstrate that motility, invasion, and contact-independent growth of PDAC cells all increase following CX3CL1 exposure, and that antagonism of CX3CR1 by the inhibitor JMS-17-2 reduces each of these phenotypes and correlates with a downregulation of AKT phosphorylation. These data suggest that PDAC tumor cell migration and growth, elements critical in metastatic progression, may susceptible to pharmacologic intervention. 相似文献
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Ye Yuan Jing‐Yi Jiang Jia‐Mei Wang Jia Sun Chao Li Bao‐Qin Liu Jing Yan Xiao‐Na Meng Hua‐Qin Wang 《Journal of cellular and molecular medicine》2019,23(8):5006-5016
BAG3 is constitutively expressed in multiple types of cancer cells and its high expression is associated with tumour progression and poor prognosis of PDAC . However, little is known about the role of BAG3 in the regulation of stromal microenvironment of PDAC. The current study demonstrated that beside PDAC tumour cells, BAG3 was also expressed in some activated stroma cells in PDAC tissue, as well as in activated PSCs. In addition, the current study demonstrated that BAG3 expression in PSCs was involved in maintenance of PSCs activation and promotion of PDACs invasion via releasing multiple cytokines. The current study demonstrated that BAG3‐positive PSCs promoted invasion of PDACs via IL‐8, MCP1, TGF‐β2 and IGFBP2 in a paracrine manner. Furthermore, BAG3 sustained PSCs activation through IL‐6, TGF‐β2 and IGFBP2 in an autocrine manner. Thereby, the current study provides a new insight into the involvement of BAG3 in remodelling of stromal microenvironment favourable for malignant progression of PDAC, indicating that BAG3 might serve as a potential target for anti‐fibrosis of PDAC. 相似文献