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10.1111/bph.13102

http://scihub22266oqcxt.onion/10.1111/bph.13102
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C4439874!4439874!25631332
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suck abstract from ncbi


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pmid25631332      Br+J+Pharmacol 2015 ; 172 (11): 2769-81
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  • Pharmacological methyl group donors block skeletal metastasis in vitro and in vivo #MMPMID25631332
  • Shukeir N; Stefanska B; Parashar S; Chik F; Arakelian A; Szyf M; Rabbani SA
  • Br J Pharmacol 2015[Jun]; 172 (11): 2769-81 PMID25631332show ga
  • Background and Purpose: DNA hypomethylation was previously implicated in metastasis. In the present study, we examined whether methyl supplementation with the universal methyl donor S-adenosylmethionine (SAM) inhibits prostate cancer associated skeletal metastasis. Experimental Approach: Highly invasive human prostate cancer cells PC-3 and DU-145 were treated with vehicle alone, S-adenosylhomocysteine (SAH) or SAM and their effects on tumour cell proliferation, invasion, migration and colony formation were monitored. For in vivo studies, control (SAH) and SAM-treated PC-3 cells were injected into the tibia of Fox chase SCID mice and skeletal lesions were determined by X-ray and ?CT. To understand possible mechanisms involved, we delineated the effect of SAM on the genome-wide methylation profile of PC-3 cells. Key Results: Treatment with SAM resulted in a dose-dependent inhibition of tumour cell proliferation, invasion, cell migration, colony formation and cell cycle characteristics. Animals injected with 250??M SAM-treated cells developed significantly smaller skeletal lesions, which were associated with increases in bone volume to tumour volume ratio and connectivity density as well as decreased trabecular spacing. Genome-wide methylation analysis showed differential methylation in several key signalling pathways implicated in prostate cancer including the signal transducer and activator of transcription 3 (STAT3) pathway. A selective STAT3 inhibitor decreased tumour cell invasion, effects which were less pronounced as compared with SAM. Conclusions and Implications: These studies provide a possible mechanism for the role of DNA demethylation in the development of skeletal metastasis and a rationale for the use of hypermethylation pharmacological agents to impede the development and progression of skeletal metastasis.
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