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10.1080/15384047.2015.1016658 http://scihub22266oqcxt.onion/10.1080/15384047.2015.1016658 C4622576!4622576!25778879     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       Cancer+Biol+Ther 2015 ; 16 (3): 466-76 Nephropedia Template TP {{tp|p=25778879|t=2015. Inhibition of autophagy overcomes glucocorticoid resistance in lymphoid malignant cells |pdf=|usr=}}{{25778879}} gab.com Text Inhibition of autophagy overcomes glucocorticoid resistance in lymphoid malignant cells JO: Cancer Biol Ther http://www.kidney.de/pget.php?&tw=1&pmid=25778879 #FOAvip Glucocorticoid (GC) resistance remains a major obstacle to successful treatment of lymphoid malignancies. Till now, the precise mechanism of GC resistance remains unclear. In the present study, dexamethasone (Dex) inhibited cell proliferation, arrested cell cycle in G0/G1-phase, and induced apoptosis in Dex-sensitive acute lymphoblastic leukemia cells. However, Dex failed to cause cell death in Dex-resistant lymphoid malignant cells. Intriguingly, we found that autophagy was induced by Dex in resistant cells, as indicated by autophagosomes formation, LC3-I to LC3-II conversion, p62 degradation, and formation of acidic autophagic vacuoles. Moreover, the results showed that Dex reduced the activity of mTOR pathway, as determined by decreased phosphorylation levels of mTOR, Akt, P70S6K and 4E-BP1 in resistant cells. Inhibition of autophagy by either chloroquine (CQ) or 3-methyladenine (3-MA) overcame Dex-resistance in lymphoid malignant cells by increasing apoptotic cell death in vitro. Consistently, inhibition of autophagy by stably knockdown of Beclin1 sensitized Dex-resistant lymphoid malignant cells to induction of apoptosis in vivo. Thus, inhibition of autophagy has the potential to improve lymphoid malignancy treatment by overcoming GC resistance. Twit Text FOAVip Inhibition of autophagy overcomes glucocorticoid resistance in lymphoid malignant cells ????Cancer Biol Ther http://www.kidney.de/pget.php?&tw=1&pmid=25778879 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25778879 #FOAvip English Wikipedia <ref>{{Cite pmid|25778879}}</ref> Inhibition of autophagy overcomes glucocorticoid resistance in lymphoid malignant cells #MMPMID25778879 Jiang L; Xu L; Xie J; Li S; Guan Y; Zhang Y; Hou Z; Guo T; Shu X; Wang C; Fan W; Si Y; Yang Y; Kang Z; Fang M; Liu Q Cancer Biol Ther 2015[Mar]; 16 (3): 466-76 PMID25778879show ga Glucocorticoid (GC) resistance remains a major obstacle to successful treatment of lymphoid malignancies. Till now, the precise mechanism of GC resistance remains unclear. In the present study, dexamethasone (Dex) inhibited cell proliferation, arrested cell cycle in G0/G1-phase, and induced apoptosis in Dex-sensitive acute lymphoblastic leukemia cells. However, Dex failed to cause cell death in Dex-resistant lymphoid malignant cells. Intriguingly, we found that autophagy was induced by Dex in resistant cells, as indicated by autophagosomes formation, LC3-I to LC3-II conversion, p62 degradation, and formation of acidic autophagic vacuoles. Moreover, the results showed that Dex reduced the activity of mTOR pathway, as determined by decreased phosphorylation levels of mTOR, Akt, P70S6K and 4E-BP1 in resistant cells. Inhibition of autophagy by either chloroquine (CQ) or 3-methyladenine (3-MA) overcame Dex-resistance in lymphoid malignant cells by increasing apoptotic cell death in vitro. Consistently, inhibition of autophagy by stably knockdown of Beclin1 sensitized Dex-resistant lymphoid malignant cells to induction of apoptosis in vivo. Thus, inhibition of autophagy has the potential to improve lymphoid malignancy treatment by overcoming GC resistance. äInhibition of autophagy overcomes glucocorticoid resistance in lymphoi(epmc).pdf DeepDyve Pubget Overpricing