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10.1016/j.ceca.2020.102307 http://scihub22266oqcxt.onion/10.1016/j.ceca.2020.102307 33080445!ä!33080445 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Calcium 2020 ; 92 (ä): 102307 Nephropedia Template TP {{tp|p=33080445|t=2020. Inhibition of TRPM7 with waixenicin A reduces glioblastoma cellular functions |pdf=|usr=}}{{33080445}} gab.com Text Inhibition of TRPM7 with waixenicin A reduces glioblastoma cellular functions JO: Cell Calcium http://www.kidney.de/pget.php?&tw=1&pmid=33080445 #FOAvip Glioblastoma (GBM) is the most common malignant primary brain tumour originating in the CNS. Median patient survival is <15 months with standard treatment which consists of surgery alongside radiation therapy and temozolomide chemotherapy. However, because of the aggressive nature of GBM, and the significant toxicity of these adjuvant therapies, long-term therapeutic effects are unsatisfactory. Thus, there is urgency to identify new drug targets for GBM. Recent evidence shows that the transient receptor potential melastatin 7 (TRPM7) cation channel is aberrantly upregulated in GBM and its inhibition leads to reduction of GBM cellular functions. This suggests that TRPM7 may be a potential drug target for GBM treatment. In this study, we assessed the effects of the specific TRPM7 antagonist waixenicin A on human GBM cell lines U87 or U251 both in vitro and in vivo. First, we demonstrated in vitro that application of waixenicin A reduced TRPM7 protein expression and inhibited the TRPM7-like currents in GBM cells. We also observed reduction of GBM cell viability, migration, and invasion. Using an intracranial xenograft GBM mouse model, we showed that with treatment of waixenicin A, there was increased cleaved caspase 3 activity, alongside reduction in Ki-67, cofilin, and Akt activity in vivo. Together, these data demonstrate higher GBM cell apoptosis, and lower proliferation, migration, invasion and survivability following treatment with waixenicin A. Twit Text FOAVip Inhibition of TRPM7 with waixenicin A reduces glioblastoma cellular functions ????Cell Calcium http://www.kidney.de/pget.php?&tw=1&pmid=33080445 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33080445 #FOAvip English Wikipedia <ref>{{Cite pmid|33080445}}</ref> Inhibition of TRPM7 with waixenicin A reduces glioblastoma cellular functions #MMPMID33080445 Wong R; Gong H; Alanazi R; Bondoc A; Luck A; Sabha N; Horgen FD; Fleig A; Rutka JT; Feng ZP; Sun HS Cell Calcium 2020[Dec]; 92 (ä): 102307 PMID33080445show ga Glioblastoma (GBM) is the most common malignant primary brain tumour originating in the CNS. Median patient survival is <15 months with standard treatment which consists of surgery alongside radiation therapy and temozolomide chemotherapy. However, because of the aggressive nature of GBM, and the significant toxicity of these adjuvant therapies, long-term therapeutic effects are unsatisfactory. Thus, there is urgency to identify new drug targets for GBM. Recent evidence shows that the transient receptor potential melastatin 7 (TRPM7) cation channel is aberrantly upregulated in GBM and its inhibition leads to reduction of GBM cellular functions. This suggests that TRPM7 may be a potential drug target for GBM treatment. In this study, we assessed the effects of the specific TRPM7 antagonist waixenicin A on human GBM cell lines U87 or U251 both in vitro and in vivo. First, we demonstrated in vitro that application of waixenicin A reduced TRPM7 protein expression and inhibited the TRPM7-like currents in GBM cells. We also observed reduction of GBM cell viability, migration, and invasion. Using an intracranial xenograft GBM mouse model, we showed that with treatment of waixenicin A, there was increased cleaved caspase 3 activity, alongside reduction in Ki-67, cofilin, and Akt activity in vivo. Together, these data demonstrate higher GBM cell apoptosis, and lower proliferation, migration, invasion and survivability following treatment with waixenicin A. |Acetates/administration & dosage/*pharmacology[MESH] |Actin Depolymerizing Factors/metabolism[MESH] |Animals[MESH] |Brain Neoplasms/*metabolism/*pathology[MESH] |Caspase 3/metabolism[MESH] |Cell Line, Tumor[MESH] |Cell Movement/drug effects[MESH] |Cell Survival/drug effects[MESH] |Diterpenes/administration & dosage/*pharmacology[MESH] |Female[MESH] |Glioblastoma/*metabolism/*pathology[MESH] |Humans[MESH] |Ki-67 Antigen/metabolism[MESH] |Mice, Inbred NOD[MESH] |Mice, SCID[MESH] |Models, Biological[MESH] |Neoplasm Invasiveness[MESH] |Protein Serine-Threonine Kinases/*antagonists & inhibitors/metabolism[MESH] |Proto-Oncogene Proteins c-akt/metabolism[MESH] |TRPM Cation Channels/*antagonists & inhibitors/metabolism[MESH]Inhibition of TRPM7 with waixenicin A reduces glioblastoma cellular fu(epmc).pdf DeepDyve Pubget Overpricing