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10.18632/oncotarget.8651 http://scihub22266oqcxt.onion/10.18632/oncotarget.8651 C5094980!5094980 !27074570     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27074570 &cmd=llinks): Failed to open stream: HTTP request failed! 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Sulfasalazine impacts on ferroptotic cell death and alleviates the tumor microenvironment and glioma-induced brain edema |pdf=|usr=}}{{27074570 }} gab.com Text Sulfasalazine impacts on ferroptotic cell death and alleviates the tumor microenvironment and glioma-induced brain edema JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27074570 #FOAvip The glutamate transporter xCT (SCL7a11, system Xc-, SXC) is an emerging key player in glutamate/cysteine/glutathione homeostasis in the brain and in cancer. xCT expression correlates with the grade of malignancy. Here, we report on the use of the U.S. Food and Drug Administration and EMA-approved xCT inhibitor, sulfasalazine (SAS) in gliomas. SAS does not affect cell viability in gliomas at concentrations below 200 µM. At higher concentrations SAS becomes gliomatoxic. Mechanistically SAS inhibits xCT and induces ferroptotic cell death in glioma cells. There is no evidence for impact on autophagic flux following SAS application. However, SAS can potentiate the efficacy of the standard chemotherapeutic and autophagy-inducing agent temozolomide (Temcat, Temodal or Temodar®). We also investigated SAS in non-transformed cellular constituents of the brain. Neurons and brain tissue are almost non-responding to SAS whereas isolated astrocytes are less sensitive towards SAS toxicity compared to gliomas. In vivo SAS treatment does not affect experimental tumor growth and treated animals revealed comparable tumor volume as untreated controls. However, SAS treatment resulted in reduced glioma-derived edema and, hence, total tumor volume burden as revealed by T2-weighted magnetic resonance imaging. Altogether, we show that SAS can be utilized for targeting the glutamate antiporter xCT activity as a tumor microenvironment-normalizing drug, while crucial cytotoxic effects in brain tumors are minor. Twit Text FOAVip Sulfasalazine impacts on ferroptotic cell death and alleviates the tumor microenvironment and glioma-induced brain edema ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27074570 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27074570 #FOAvip English Wikipedia <ref>{{Cite pmid|27074570 }}</ref> Sulfasalazine impacts on ferroptotic cell death and alleviates the tumor microenvironment and glioma-induced brain edema #MMPMID27074570 Sehm T ; Fan Z ; Ghoochani A ; Rauh M ; Engelhorn T ; Minakaki G ; Dörfler A ; Klucken J ; Buchfelder M ; Eyüpoglu IY ; Savaskan N Oncotarget 2016[Jun]; 7 (24 ): 36021-36033 PMID27074570 show ga The glutamate transporter xCT (SCL7a11, system Xc-, SXC) is an emerging key player in glutamate/cysteine/glutathione homeostasis in the brain and in cancer. xCT expression correlates with the grade of malignancy. Here, we report on the use of the U.S. Food and Drug Administration and EMA-approved xCT inhibitor, sulfasalazine (SAS) in gliomas. SAS does not affect cell viability in gliomas at concentrations below 200 µM. At higher concentrations SAS becomes gliomatoxic. Mechanistically SAS inhibits xCT and induces ferroptotic cell death in glioma cells. There is no evidence for impact on autophagic flux following SAS application. However, SAS can potentiate the efficacy of the standard chemotherapeutic and autophagy-inducing agent temozolomide (Temcat, Temodal or Temodar®). We also investigated SAS in non-transformed cellular constituents of the brain. Neurons and brain tissue are almost non-responding to SAS whereas isolated astrocytes are less sensitive towards SAS toxicity compared to gliomas. In vivo SAS treatment does not affect experimental tumor growth and treated animals revealed comparable tumor volume as untreated controls. However, SAS treatment resulted in reduced glioma-derived edema and, hence, total tumor volume burden as revealed by T2-weighted magnetic resonance imaging. Altogether, we show that SAS can be utilized for targeting the glutamate antiporter xCT activity as a tumor microenvironment-normalizing drug, while crucial cytotoxic effects in brain tumors are minor. |Amino Acid Transport System X-AG/antagonists & inhibitors/metabolism [MESH] |Animals [MESH] |Animals, Newborn [MESH] |Anti-Inflammatory Agents, Non-Steroidal/pharmacology [MESH] |Brain Edema/diagnostic imaging/etiology/*prevention & control [MESH] |Brain Neoplasms/complications/*drug therapy/metabolism [MESH] |Cell Death/drug effects [MESH] |Cell Line, Tumor [MESH] |Cell Survival/drug effects [MESH] |Cells, Cultured [MESH] |Dacarbazine/analogs & derivatives/pharmacology [MESH] |Dose-Response Relationship, Drug [MESH] |Drug Synergism [MESH] |Glioma/complications/*drug therapy/metabolism [MESH] |Humans [MESH] |Magnetic Resonance Imaging [MESH] |Rats, Wistar [MESH] |Sulfasalazine/*pharmacology [MESH] |Temozolomide [MESH]Sulfasalazine impacts on ferroptotic cell death and alleviates the tum(epmc).pdf DeepDyve Pubget Overpricing