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10.1158/0008-5472.CAN-15-2534 http://scihub22266oqcxt.onion/10.1158/0008-5472.CAN-15-2534 C4930686!4930686 !27216187     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27216187 &cmd=llinks): Failed to open stream: HTTP request failed! 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Mitochondria-Targeted Analogues of Metformin Exhibit Enhanced Antiproliferative and Radiosensitizing Effects in Pancreatic Cancer Cells |pdf=|usr=}}{{27216187 }} gab.com Text Mitochondria-Targeted Analogues of Metformin Exhibit Enhanced Antiproliferative and Radiosensitizing Effects in Pancreatic Cancer Cells JO: Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=27216187 #FOAvip Metformin (Met) is an approved antidiabetic drug currently being explored for repurposing in cancer treatment based on recent evidence of its apparent chemopreventive properties. Met is weakly cationic and targets the mitochondria to induce cytotoxic effects in tumor cells, albeit not very effectively. We hypothesized that increasing its mitochondria-targeting potential by attaching a positively charged lipophilic substituent would enhance the antitumor activity of Met. In pursuit of this question, we synthesized a set of mitochondria-targeted Met analogues (Mito-Mets) with varying alkyl chain lengths containing a triphenylphosphonium cation (TPP(+)). In particular, the analogue Mito-Met10, synthesized by attaching TPP(+) to Met via a 10-carbon aliphatic side chain, was nearly 1,000 times more efficacious than Met at inhibiting cell proliferation in pancreatic ductal adenocarcinoma (PDAC). Notably, in PDAC cells, Mito-Met10 potently inhibited mitochondrial complex I, stimulating superoxide and AMPK activation, but had no effect in nontransformed control cells. Moreover, Mito-Met10 potently triggered G1 cell-cycle phase arrest in PDAC cells, enhanced their radiosensitivity, and more potently abrogated PDAC growth in preclinical mouse models, compared with Met. Collectively, our findings show how improving the mitochondrial targeting of Met enhances its anticancer activities, including aggressive cancers like PDAC in great need of more effective therapeutic options. Cancer Res; 76(13); 3904-15. ©2016 AACR. Twit Text FOAVip Mitochondria-Targeted Analogues of Metformin Exhibit Enhanced Antiproliferative and Radiosensitizing Effects in Pancreatic Cancer Cells ????Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=27216187 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27216187 #FOAvip English Wikipedia <ref>{{Cite pmid|27216187 }}</ref> Mitochondria-Targeted Analogues of Metformin Exhibit Enhanced Antiproliferative and Radiosensitizing Effects in Pancreatic Cancer Cells #MMPMID27216187 Cheng G ; Zielonka J ; Ouari O ; Lopez M ; McAllister D ; Boyle K ; Barrios CS ; Weber JJ ; Johnson BD ; Hardy M ; Dwinell MB ; Kalyanaraman B Cancer Res 2016[Jul]; 76 (13 ): 3904-15 PMID27216187 show ga Metformin (Met) is an approved antidiabetic drug currently being explored for repurposing in cancer treatment based on recent evidence of its apparent chemopreventive properties. Met is weakly cationic and targets the mitochondria to induce cytotoxic effects in tumor cells, albeit not very effectively. We hypothesized that increasing its mitochondria-targeting potential by attaching a positively charged lipophilic substituent would enhance the antitumor activity of Met. In pursuit of this question, we synthesized a set of mitochondria-targeted Met analogues (Mito-Mets) with varying alkyl chain lengths containing a triphenylphosphonium cation (TPP(+)). In particular, the analogue Mito-Met10, synthesized by attaching TPP(+) to Met via a 10-carbon aliphatic side chain, was nearly 1,000 times more efficacious than Met at inhibiting cell proliferation in pancreatic ductal adenocarcinoma (PDAC). Notably, in PDAC cells, Mito-Met10 potently inhibited mitochondrial complex I, stimulating superoxide and AMPK activation, but had no effect in nontransformed control cells. Moreover, Mito-Met10 potently triggered G1 cell-cycle phase arrest in PDAC cells, enhanced their radiosensitivity, and more potently abrogated PDAC growth in preclinical mouse models, compared with Met. Collectively, our findings show how improving the mitochondrial targeting of Met enhances its anticancer activities, including aggressive cancers like PDAC in great need of more effective therapeutic options. Cancer Res; 76(13); 3904-15. ©2016 AACR. |Animals [MESH] |Apoptosis/drug effects/radiation effects [MESH] |Blotting, Western [MESH] |Carcinoma, Pancreatic Ductal/drug therapy/*pathology/radiotherapy [MESH] |Cell Cycle/drug effects/radiation effects [MESH] |Cell Proliferation/drug effects/radiation effects [MESH] |Chemoradiotherapy [MESH] |Humans [MESH] |Hypoglycemic Agents/chemistry/pharmacology [MESH] |Metformin/chemistry/*pharmacology [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Transgenic [MESH] |Mitochondria/*drug effects/pathology [MESH] |Pancreatic Neoplasms/drug therapy/*pathology/radiotherapy [MESH] |Radiation-Sensitizing Agents/chemistry/*pharmacology [MESH] |Signal Transduction [MESH] |Superoxides [MESH] |Tumor Cells, Cultured [MESH]Mitochondria-Targeted Analogues of Metformin Exhibit Enhanced Antiprol(epmc).pdf DeepDyve Pubget Overpricing