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.

10.1155/2021/5558618 http://scihub22266oqcxt.onion/10.1155/2021/5558618 34136065!8177987!34136065     free     free     free Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 253.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 253.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 253.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 253.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 253.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 286.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 286.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 286.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 286.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oxid+Med+Cell+Longev 2021 ; 2021 (ä): 5558618 Nephropedia Template TP {{tp|p=34136065|t=2021. Hypoxia Induced by Cobalt Chloride Triggers Autophagic Apoptosis of Human and Mouse Drug-Resistant Glioblastoma Cells through Targeting the PI3K-AKT-mTOR Signaling Pathway |pdf=|usr=}}{{34136065}} gab.com Text Hypoxia Induced by Cobalt Chloride Triggers Autophagic Apoptosis of Human and Mouse Drug-Resistant Glioblastoma Cells through Targeting the PI3K-AKT-mTOR Signaling Pathway JO: Oxid Med Cell Longev http://www.kidney.de/pget.php?&tw=1&pmid=34136065 #FOAvip Glioblastoma multiforme (GBM) is the most aggressive brain tumor. Drug resistance mainly drives GBM patients to poor prognoses because drug-resistant glioblastoma cells highly defend against apoptotic insults. This study was designed to evaluate the effects of cobalt chloride (CoCl(2)) on hypoxic stress, autophagy, and resulting apoptosis of human and mouse drug-resistant glioblastoma cells. Treatment of drug-resistant glioblastoma cells with CoCl(2) increased levels of hypoxia-inducible factor- (HIF-) 1alpha and triggered hypoxic stress. In parallel, the CoCl(2)-induced hypoxia decreased mitochondrial ATP synthesis, cell proliferation, and survival in chemoresistant glioblastoma cells. Interestingly, CoCl(2) elevated the ratio of light chain (LC)3-II over LC3-I in TMZ-resistant glioblastoma cells and subsequently induced cell autophagy. Analyses by loss- and gain-of-function strategies further confirmed the effects of the CoCl(2)-induced hypoxia on autophagy of drug-resistant glioblastoma cells. Furthermore, knocking down HIF-1alpha concurrently lessened CoCl(2)-induced cell autophagy. As to the mechanisms, the CoCl(2)-induced hypoxia decreased levels of phosphoinositide 3-kinase (PI3K) and successive phosphorylations of AKT and mammalian target of rapamycin (mTOR) in TMZ-resistant glioblastoma cells. Interestingly, long-term exposure of human chemoresistant glioblastoma cells to CoCl(2) sequentially triggered activation of caspases-3 and -6, DNA fragmentation, and cell apoptosis. However, pretreatment with 3-methyladenine, an inhibitor of autophagy, significantly attenuated the CoCl(2)-induced autophagy and subsequent apoptotic insults. Taken together, this study showed that long-term treatment with CoCl(2) can induce hypoxia and subsequent autophagic apoptosis of drug-resistant glioblastoma cells via targeting the PI3K-AKT-mTOR pathway. Thus, combined with traditional prescriptions, CoCl(2)-induced autophagic apoptosis can be clinically applied as a de novo strategy for therapy of drug-resistant GBM patients. Twit Text FOAVip Hypoxia Induced by Cobalt Chloride Triggers Autophagic Apoptosis of Human and Mouse Drug-Resistant Glioblastoma Cells through Targeting the PI3K-AKT-mTOR Signaling Pathway ????Oxid Med Cell Longev http://www.kidney.de/pget.php?&tw=1&pmid=34136065 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34136065 #FOAvip English Wikipedia <ref>{{Cite pmid|34136065}}</ref> Hypoxia Induced by Cobalt Chloride Triggers Autophagic Apoptosis of Human and Mouse Drug-Resistant Glioblastoma Cells through Targeting the PI3K-AKT-mTOR Signaling Pathway #MMPMID34136065 Lee YW; Cherng YG; Yang ST; Liu SH; Chen TL; Chen RM Oxid Med Cell Longev 2021[]; 2021 (ä): 5558618 PMID34136065show ga Glioblastoma multiforme (GBM) is the most aggressive brain tumor. Drug resistance mainly drives GBM patients to poor prognoses because drug-resistant glioblastoma cells highly defend against apoptotic insults. This study was designed to evaluate the effects of cobalt chloride (CoCl(2)) on hypoxic stress, autophagy, and resulting apoptosis of human and mouse drug-resistant glioblastoma cells. Treatment of drug-resistant glioblastoma cells with CoCl(2) increased levels of hypoxia-inducible factor- (HIF-) 1alpha and triggered hypoxic stress. In parallel, the CoCl(2)-induced hypoxia decreased mitochondrial ATP synthesis, cell proliferation, and survival in chemoresistant glioblastoma cells. Interestingly, CoCl(2) elevated the ratio of light chain (LC)3-II over LC3-I in TMZ-resistant glioblastoma cells and subsequently induced cell autophagy. Analyses by loss- and gain-of-function strategies further confirmed the effects of the CoCl(2)-induced hypoxia on autophagy of drug-resistant glioblastoma cells. Furthermore, knocking down HIF-1alpha concurrently lessened CoCl(2)-induced cell autophagy. As to the mechanisms, the CoCl(2)-induced hypoxia decreased levels of phosphoinositide 3-kinase (PI3K) and successive phosphorylations of AKT and mammalian target of rapamycin (mTOR) in TMZ-resistant glioblastoma cells. Interestingly, long-term exposure of human chemoresistant glioblastoma cells to CoCl(2) sequentially triggered activation of caspases-3 and -6, DNA fragmentation, and cell apoptosis. However, pretreatment with 3-methyladenine, an inhibitor of autophagy, significantly attenuated the CoCl(2)-induced autophagy and subsequent apoptotic insults. Taken together, this study showed that long-term treatment with CoCl(2) can induce hypoxia and subsequent autophagic apoptosis of drug-resistant glioblastoma cells via targeting the PI3K-AKT-mTOR pathway. Thus, combined with traditional prescriptions, CoCl(2)-induced autophagic apoptosis can be clinically applied as a de novo strategy for therapy of drug-resistant GBM patients. |Animals[MESH] |Apoptosis[MESH] |Brain Neoplasms/*complications/pathology[MESH] |Cell Hypoxia/*genetics[MESH] |Cell Line, Tumor[MESH] |Cell Proliferation[MESH] |Cobalt/*adverse effects[MESH] |Glioblastoma/*complications/pathology[MESH] |Humans[MESH] |Mice[MESH] |Phosphatidylinositol 3-Kinase/*metabolism[MESH] |Phosphatidylinositol 3-Kinases/*metabolism[MESH]Hypoxia Induced by Cobalt Chloride Triggers Autophagic Apoptosis of Hu(epmc).pdf DeepDyve Pubget Overpricing