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10.3892/ol.2016.4870 http://scihub22266oqcxt.onion/10.3892/ol.2016.4870 C4998146!4998146 !27602117     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27602117 &cmd=llinks): Failed to open stream: HTTP request failed! 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Dihydroartemisinin induces endothelial cell anoikis through the activation of the JNK signaling pathway |pdf=|usr=}}{{27602117 }} gab.com Text Dihydroartemisinin induces endothelial cell anoikis through the activation of the JNK signaling pathway JO: Oncol Lett http://www.kidney.de/pget.php?&tw=1&pmid=27602117 #FOAvip Angiogenesis is required for the growth and metastasis of solid tumors. The anti-malarial agent dihydroartemisinin (DHA) demonstrates potent anti-angiogenic activity, but the underlying molecular mechanisms are not yet fully understood. During the process of angiogenesis, endothelial cells migrating from existing capillaries may undergo programmed cell death after detaching from the extracellular matrix, a process that is defined as anchorage-dependent apoptosis or anoikis. In the present study, DHA-induced cell death was compared in human umbilical vein endothelial cells (HUVECs) cultured in suspension and attached to culture plates. In suspended HUVECs, the cell viability was decreased and apoptosis was increased with the treatment of 50 µM DHA for 5 h, while the same treatment did not affect the attached HUVECs. In addition, 50 µM DHA increased the phosphorylation of c-Jun N-terminal kinase (JNK) in suspended HUVECs, but not in attached HUVECs, for up to 5 h of treatment. The JNK inhibitor, SP600125, reversed DHA-induced cell death in suspended HUVECs, suggesting that the JNK pathway may mediate DHA-induced endothelial cell anoikis. The data from the present study indicates a novel mechanism for understanding the anti-angiogenic effects of DHA, which may be used as a component for chemotherapy. Twit Text FOAVip Dihydroartemisinin induces endothelial cell anoikis through the activation of the JNK signaling pathway ????Oncol Lett http://www.kidney.de/pget.php?&tw=1&pmid=27602117 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27602117 #FOAvip English Wikipedia <ref>{{Cite pmid|27602117 }}</ref> Dihydroartemisinin induces endothelial cell anoikis through the activation of the JNK signaling pathway #MMPMID27602117 Zhang J ; Guo L ; Zhou X ; Dong F ; Li L ; Cheng Z ; Xu Y ; Liang J ; Xie Q ; Liu J Oncol Lett 2016[Sep]; 12 (3 ): 1896-1900 PMID27602117 show ga Angiogenesis is required for the growth and metastasis of solid tumors. The anti-malarial agent dihydroartemisinin (DHA) demonstrates potent anti-angiogenic activity, but the underlying molecular mechanisms are not yet fully understood. During the process of angiogenesis, endothelial cells migrating from existing capillaries may undergo programmed cell death after detaching from the extracellular matrix, a process that is defined as anchorage-dependent apoptosis or anoikis. In the present study, DHA-induced cell death was compared in human umbilical vein endothelial cells (HUVECs) cultured in suspension and attached to culture plates. In suspended HUVECs, the cell viability was decreased and apoptosis was increased with the treatment of 50 µM DHA for 5 h, while the same treatment did not affect the attached HUVECs. In addition, 50 µM DHA increased the phosphorylation of c-Jun N-terminal kinase (JNK) in suspended HUVECs, but not in attached HUVECs, for up to 5 h of treatment. The JNK inhibitor, SP600125, reversed DHA-induced cell death in suspended HUVECs, suggesting that the JNK pathway may mediate DHA-induced endothelial cell anoikis. The data from the present study indicates a novel mechanism for understanding the anti-angiogenic effects of DHA, which may be used as a component for chemotherapy. äDihydroartemisinin induces endothelial cell anoikis through the activa(epmc).pdf DeepDyve Pubget Overpricing