絞り込み

16735

広告

Aspirin impairs acetyl-coenzyme A metabolism in redox-compromised yeast cells.

著者 Farrugia G , Azzopardi M , Saliba C , Grech G , Gross AS , Pistolic J , Benes V , Vassallo N , Borg J , Madeo F , Eisenberg T , Balzan R
Sci Rep.2019 Apr 16 ; 9(1):6152.
この記事をPubMed上で見るPubMedで表示
この記事をGoogle翻訳上で見る Google翻訳で開く

スターを付ける スターを付ける     (1view , 0users)

Full Text Sources

Aspirin is a widely used anti-inflammatory and antithrombotic drug also known in recent years for its promising chemopreventive antineoplastic properties, thought to be mediated in part by its ability to induce apoptotic cell death. However, the full range of mechanisms underlying aspirin's cancer-preventive properties is still elusive. In this study, we observed that aspirin impaired both the synthesis and transport of acetyl-coenzyme A (acetyl-CoA) into the mitochondria of manganese superoxide dismutase (MnSOD)-deficient Saccharomyces cerevisiae EG110 yeast cells, but not of the wild-type cells, grown aerobically in ethanol medium. This occurred at both the gene level, as indicated by microarray and qRT-PCR analyses, and at the protein level as indicated by enzyme assays. These results show that in redox-compromised MnSOD-deficient yeast cells, but not in wild-type cells, aspirin starves the mitochondria of acetyl-CoA and likely causes energy failure linked to mitochondrial damage, resulting in cell death. Since acetyl-CoA is one of the least-studied targets of aspirin in terms of the latter's propensity to prevent cancer, this work may provide further mechanistic insight into aspirin's chemopreventive behavior with respect to early stage cancer cells, which tend to have downregulated MnSOD and are also redox-compromised.
PMID: 30992471 [PubMed - in process]
印刷用ページを開く Endnote用テキストダウンロード