Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1371/journal.pone.0200452 http://scihub22266oqcxt.onion/10.1371/journal.pone.0200452 C6040758!6040758!29995950     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+One 2018 ; 13 (7): ä Nephropedia Template TP {{tp|p=29995950|t=2018. VEGFC/VEGFR3 axis mediates TGF?1-induced epithelial-to-mesenchymal transition in non-small cell lung cancer cells |pdf=|usr=}}{{29995950}} gab.com Text VEGFC/VEGFR3 axis mediates TGF 1-induced epithelial-to-mesenchymal transition in non-small cell lung cancer cells JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=29995950 #FOAvip In the tumor progression, transforming growth factor ?1 (TGF?1) plays a critical role in tumorigenesis as well as metastasis. It is known that high plasma level of TGF?1 in patients with advanced non-small cell lung cancer (NSCLC) is correlated with poor prognostics. In addition, the generation of cancer stem-like cells is associated with metastasis, drug resistance, and tumor recurrence, which also lead to poor outcomes in NSCLC patients. However, it remains unclear how TGF?1 promotes NSCLC cells to acquire stem-like properties and accelerate tumor metastasis. In our study, we found that short term TGF?1 treatment resulted in a significant epithelial-mesenchymal transition (EMT) morphological change in TGF?1?sensitive NSCLC cells but not in insensitive cells. Western blotting confirmed increased Vimentin and reduced E-Cadherin protein expression after TGF?1 treatment in A549, NCI-H1993, and NCI-H358 cells. TGF?1 incubation dramatically decreased in vitro cell proliferation and increased cell invasion in TGF?1?sensitive NSCLC cells but not in NCI-H1975, NCI-H1650, and HCC827 cells. Moreover, TGF?1 was able to enhance the mRNA expression of Oct4, Nanog and Sox2 and drastically increased anchorage-independent colony formation in TGF?1?sensitive NSCLC cells, suggesting the acquisition of cancer stem-like properties. Interestingly, we found that vascular endothelial growth factor receptor 3 (VEGFR3) mRNA expression was significantly elevated in TGF?1?sensitive NSCLC cells compared to insensitive cells. And TGF?1 was capable of inducing VEGF-C gene expression. Pharmacological blocking TGF? type I receptor kinase (ALK5) significantly inhibited TGF?1-induced VEGF-C expression. Silencing of ALK5 by siRNA also dramatically reduced TGF?1-induced VEGF-C expression in TGF?1?sensitive NSCLC cells. Therefore, TGF?1 contributes for NSCLC metastasis through promoting EMT, generation of high invasive cancer cells with stem-like properties, and increasing VEGF-C expression. Blocking TGF? pathway is a potential therapeutic target in human non-small cell lung cancer. Twit Text FOAVip VEGFC/VEGFR3 axis mediates TGF 1-induced epithelial-to-mesenchymal transition in non-small cell lung cancer cells ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=29995950 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29995950 #FOAvip English Wikipedia <ref>{{Cite pmid|29995950}}</ref> VEGFC/VEGFR3 axis mediates TGF?1-induced epithelial-to-mesenchymal transition in non-small cell lung cancer cells #MMPMID29995950 Duan L; Ye L; Zhuang L; Zou X; Liu S; Zhang Y; Zhang L; Jin C; Huang Y PLoS One 2018[]; 13 (7): ä PMID29995950show ga In the tumor progression, transforming growth factor ?1 (TGF?1) plays a critical role in tumorigenesis as well as metastasis. It is known that high plasma level of TGF?1 in patients with advanced non-small cell lung cancer (NSCLC) is correlated with poor prognostics. In addition, the generation of cancer stem-like cells is associated with metastasis, drug resistance, and tumor recurrence, which also lead to poor outcomes in NSCLC patients. However, it remains unclear how TGF?1 promotes NSCLC cells to acquire stem-like properties and accelerate tumor metastasis. In our study, we found that short term TGF?1 treatment resulted in a significant epithelial-mesenchymal transition (EMT) morphological change in TGF?1?sensitive NSCLC cells but not in insensitive cells. Western blotting confirmed increased Vimentin and reduced E-Cadherin protein expression after TGF?1 treatment in A549, NCI-H1993, and NCI-H358 cells. TGF?1 incubation dramatically decreased in vitro cell proliferation and increased cell invasion in TGF?1?sensitive NSCLC cells but not in NCI-H1975, NCI-H1650, and HCC827 cells. Moreover, TGF?1 was able to enhance the mRNA expression of Oct4, Nanog and Sox2 and drastically increased anchorage-independent colony formation in TGF?1?sensitive NSCLC cells, suggesting the acquisition of cancer stem-like properties. Interestingly, we found that vascular endothelial growth factor receptor 3 (VEGFR3) mRNA expression was significantly elevated in TGF?1?sensitive NSCLC cells compared to insensitive cells. And TGF?1 was capable of inducing VEGF-C gene expression. Pharmacological blocking TGF? type I receptor kinase (ALK5) significantly inhibited TGF?1-induced VEGF-C expression. Silencing of ALK5 by siRNA also dramatically reduced TGF?1-induced VEGF-C expression in TGF?1?sensitive NSCLC cells. Therefore, TGF?1 contributes for NSCLC metastasis through promoting EMT, generation of high invasive cancer cells with stem-like properties, and increasing VEGF-C expression. Blocking TGF? pathway is a potential therapeutic target in human non-small cell lung cancer. äVEGFC/VEGFR3 axis mediates TGF?1-induced epithelial-to-mesenchymal tra(epmc).pdf DeepDyve Pubget Overpricing