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10.1158/0008-5472.CAN-15-2534

http://scihub22266oqcxt.onion/10.1158/0008-5472.CAN-15-2534
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C4930686!4930686!27216187
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suck abstract from ncbi


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pmid27216187      Cancer+Res 2016 ; 76 (13): 3904-15
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  • Mitochondria-targeted analogs 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 PMID27216187show 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 analogs (Mito-Mets) with varying alkyl chain lengths containing a triphenylphosphonium cation (TPP+). In particular, the analog 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 non-transformed 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 to Met. Collectively, our findings show how improving the mitochondrial targeting of Met enhances its anticancer activities, including in aggressive cancers like PDAC in great need of more effective therapeutic options.
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