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10.3892/ijo.2018.4325 http://scihub22266oqcxt.onion/10.3892/ijo.2018.4325 C5873869!5873869!29568964     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 300.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 300.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 300.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Int+J+Oncol 2018 ; 52 (5): 1465-78 Nephropedia Template TP {{tp|p=29568964|t=2018. Disruption of IGF-1R signaling by a novel quinazoline derivative, HMJ-30, inhibits invasiveness and reverses epithelial-mesenchymal transition in osteosarcoma U-2 OS cells |pdf=|usr=}}{{29568964}} gab.com Text Disruption of IGF-1R signaling by a novel quinazoline derivative, HMJ-30, inhibits invasiveness and reverses epithelial-mesenchymal transition in osteosarcoma U-2 OS cells JO: Int J Oncol http://www.kidney.de/pget.php?&tw=1&pmid=29568964 #FOAvip Osteosarcoma is the most common primary malignancy of the bone and is characterized by local invasion and distant metastasis. Over the past 20 years, long-term outcomes have reached a plateau even with aggressive therapy. Overexpression of insulin-like growth factor 1 receptor (IGF-1R) is associated with tumor proliferation, invasion and migration in osteosarcoma. In the present study, our group developed a novel quinazoline derivative, 6-fluoro-2-(3-fluorophenyl)-4-(cyanoanilino)quinazoline (HMJ-30), in order to disrupt IGF-1R signaling and tumor invasiveness in osteosarcoma U-2 OS cells. Molecular modeling, immune-precipitation, western blotting and phosphorylated protein kinase sandwich ELISA assays were used to confirm this hypothesis. The results demonstrated that HMJ-30 selectively targeted the ATP-binding site of IGF-1R and inhibited its downstream phosphoinositide 3-kinase/protein kinase B, Ras/mitogen-activated protein kinase, and I?K/nuclear factor-?B signaling pathways in U-2 OS cells. HMJ-30 inhibited U-2 OS cell invasion and migration and downregulated protein levels and activities of matrix metalloproteinase (MMP)-2 and MMP-9. An increase in protein levels of tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2 was also observed. Furthermore, HMJ-30 caused U-2 OS cells to aggregate and form tight clusters, and these cells were flattened, less elongated and displayed cobblestone-like shapes. There was an increase in epithelial markers and a decrease in mesenchymal markers, indicating that the cells underwent the reverse epithelial-mesenchymal transition (EMT) process. Overall, these results demonstrated the potential molecular mechanisms underlying the effects of HMJ-30 on invasiveness and EMT in U-2 OS cells, suggesting that this compound deserves further investigation as a potential anti-osteosarcoma drug. Twit Text FOAVip Disruption of IGF-1R signaling by a novel quinazoline derivative, HMJ-30, inhibits invasiveness and reverses epithelial-mesenchymal transition in osteosarcoma U-2 OS cells ????Int J Oncol http://www.kidney.de/pget.php?&tw=1&pmid=29568964 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29568964 #FOAvip English Wikipedia <ref>{{Cite pmid|29568964}}</ref> Disruption of IGF-1R signaling by a novel quinazoline derivative, HMJ-30, inhibits invasiveness and reverses epithelial-mesenchymal transition in osteosarcoma U-2 OS cells #MMPMID29568964 Chiu YJ; Hour MJ; Jin YA; Lu CC; Tsai FJ; Chen TL; Ma H; Juan YN; Yang JS Int J Oncol 2018[May]; 52 (5): 1465-78 PMID29568964show ga Osteosarcoma is the most common primary malignancy of the bone and is characterized by local invasion and distant metastasis. Over the past 20 years, long-term outcomes have reached a plateau even with aggressive therapy. Overexpression of insulin-like growth factor 1 receptor (IGF-1R) is associated with tumor proliferation, invasion and migration in osteosarcoma. In the present study, our group developed a novel quinazoline derivative, 6-fluoro-2-(3-fluorophenyl)-4-(cyanoanilino)quinazoline (HMJ-30), in order to disrupt IGF-1R signaling and tumor invasiveness in osteosarcoma U-2 OS cells. Molecular modeling, immune-precipitation, western blotting and phosphorylated protein kinase sandwich ELISA assays were used to confirm this hypothesis. The results demonstrated that HMJ-30 selectively targeted the ATP-binding site of IGF-1R and inhibited its downstream phosphoinositide 3-kinase/protein kinase B, Ras/mitogen-activated protein kinase, and I?K/nuclear factor-?B signaling pathways in U-2 OS cells. HMJ-30 inhibited U-2 OS cell invasion and migration and downregulated protein levels and activities of matrix metalloproteinase (MMP)-2 and MMP-9. An increase in protein levels of tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2 was also observed. Furthermore, HMJ-30 caused U-2 OS cells to aggregate and form tight clusters, and these cells were flattened, less elongated and displayed cobblestone-like shapes. There was an increase in epithelial markers and a decrease in mesenchymal markers, indicating that the cells underwent the reverse epithelial-mesenchymal transition (EMT) process. Overall, these results demonstrated the potential molecular mechanisms underlying the effects of HMJ-30 on invasiveness and EMT in U-2 OS cells, suggesting that this compound deserves further investigation as a potential anti-osteosarcoma drug. äDisruption of IGF-1R signaling by a novel quinazoline derivative, HMJ-(epmc).pdf DeepDyve Pubget Overpricing