Journals / Marmara Medical Journal / 2018 / Cilt: 31 - Sayı: 2

Effect of ketone bodies on viability of human breast cancer cells (MCF-7)

Keton cisimlerinin insan meme kanseri hücrelerinde (MCF-7) canlılık üzerine etkileri

Pages
57–60
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Objective: Cancer cells exhibit an elevated glycolytic phenotype

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Objective: Cancer cells exhibit an elevated glycolytic phenotype
📊
Key Findings & Data:Objective: Cancer cells exhibit an elevated glycolytic phenotype
💡
Conclusion & Impact:Objective: Cancer cells exhibit an elevated glycolytic phenotype
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Asetoasetat · Beta-hidroksibütirat · Keton cisimleri

Abstract

Objective: Cancer cells exhibit an elevated glycolytic phenotype

Özet

Amaç: Kanser hücreleri aerobik koşullar altında Warburg etkisi

🔖

Cite This Article

KAYA, Z., YILMAZ, A. M., YALÇIN, A. S. (2018). Effect of ketone bodies on viability of human breast cancer cells (MCF-7). Marmara Medical Journal, Cilt: 31 - Sayı: 2, 57–60. https://ajindex.com/articles/284291

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (2)

  1. Skinner R, Trujillo A, Ma X, Beierle EA. Ketone bodies inhibit the viability of human neuroblastoma cells. J Pediatr Surg 2009; 44: 212-6. doi: 10.1016/j.jpedsurg.2008.10.042 Isidoro A, Martınez M, Fernandez P, et al. Alteration of the bioenergetic phenotype of mitochondria is a hallmark of breast, gastric, lung and oesophageal cancer. Biochem J 2004; 378: 17-20. doi:10.1042/BJ20031541 Kiebish MA, Han X, Cheng H, et al. Cardiolipin and electron transport chain abnormalities in mouse brain tumor mitochondria: lipidomic evidence supporting the Warburg theory of cancer. J Lipid Res 2008; 49: 2545-56. doi: 10.1194/ jlr.M800319-JLR200 Modica-Napolitano J, Singh K. Mitochondrial dysfunction in cancer. Mitochondrion 2004; 4: 755-817. doi: 10.1016/j. mito.2004.07.027 Seyfried TN. Cancer as a metabolic disease: on the origin, management, and prevention of cancer. Hoboken, NJ: Wiley, 2012. doi: 10.1093/carcin/bgt480 Maurer GD, Brucker DP, Baehr O, et al. Differential utilization of ketone bodies by neurons and glioma cell lines: a rationale for ketogenic diet as experimental glioma therapy. BMC Cancer 2015; 11: 315. doi: 10.1186/1471- 2407-11-315
  2. Poff AM, Ari C, Arnold P, Seyfried TN, D’Agostino DP. Ketone supplementation decreases tumor cell viability and prolongs survival of mice with metastatic cancer. Int J Cancer 2014; 135: 1711-20. doi: 10.1002/ijc.28809 Branco AF, Ferreira A, Simões RF, et al. Ketogenic diets: from cancer to mitochondrial diseases and beyond. Eur J Clin Invest 2016; 46: 285-98. doi: 10.1111/eci.12591 Aykin-Burns N, Ahmad IM, Zhu Y, Oberley LW, Spitz DR. Increased levels of superoxide and H2O2 mediate the differential susceptibility of cancer cells versus normal cells to glucose deprivation. Biochem J 2009; 418: 29-37. doi: 10.1042/BJ20081258 Wu GY, Thompson JR. The effect of ketone bodies on alanine and glutamine metabolism in isolated skeletal muscle from the fasted chick. Biochem J 1988; 255: 139-44. Schumacker P. Reactive oxygen species in cancer cells: live by the sword, die by the sword. Cancer Cell 2006; 10: 175- 81. doi: 10.1016/j.ccr.2006.08.015 Veech RL, Chance B, Kashiwaya Y, et al. Ketone bodies, potential therapeutic uses. IUBMB Life 2001; 51: 241-7. doi: 10.1080/152165401753311780 Noh HS, Hah YS, Nilufar R, et al. Acetoacetate protects neuronal cells from oxidative glutamate toxicity. J Neurosci Res 2006; 83: 702-9. doi: 10.1002/jnr.20736. Cos S, Recio J, Sánchez-Barceló EJ. Modulation of the length of the cell cycle time of MCF-