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Prostate cancer cells survive anti-androgen and mitochondrial metabolic inhibitors by modulating glycolysis and mitochondrial metabolic activities
The Prostate ( IF 2.6 ) Pub Date : 2021-06-25 , DOI: 10.1002/pros.24146
Hirak S Basu 1 , Nathaniel Wilganowski 1 , Samantha Robertson 1 , James M Reuben 2 , Evan N Cohen 2 , Amado Zurita 1 , Sumankalai Ramachandran 1 , Lian-Chun Xiao 3 , Mark Titus 1 , George Wilding 1
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Most cancer cells are more glycolytic even under aerobic conditions compared with their normal counterparts. Recent evidence of tumor cell metabolism, however, shows that some tumors also increase mitochondrial oxidative phosphorylation (ox-phos) at some disease states during progression and/or development of drug resistance. Our data show that anti-androgen enzalutamide (ENZA) resistant prostate cancer (PCa) cells use more mitochondrial metabolism leading to higher ox-phos as compared to the ENZA-sensitive cells and can become vulnerable to mitochondrial metabolism targeted therapies.

中文翻译:


前列腺癌细胞通过调节糖酵解和线粒体代谢活动而在抗雄激素和线粒体代谢抑制剂中存活



与正常细胞相比,大多数癌细胞即使在有氧条件下也具有更强的糖酵解能力。然而,肿瘤细胞代谢的最新证据表明,在某些疾病状态下,在耐药性的进展和/或发展过程中,一些肿瘤也会增加线粒体氧化磷酸化(ox-phos)。我们的数据显示,与 ENZA 敏感细胞相比,抗雄激素恩杂鲁胺 (ENZA) 耐药性前列腺癌 (PCa) 细胞使用更多的线粒体代谢,导致更高的氧化磷,并且可能容易受到线粒体代谢靶向治疗的影响。
更新日期:2021-07-20
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