Cancer Biol

Ther 2008, 7:1555–1560.PubMedCrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions MEI carried out the most experimental work. VH performed the sample collection and Ki67 assays. PM performed the sample collections, provided clinical data. PM, FM, and EW were responsible for the design of the study and its coordination. PM, EW, and FM wrote the manuscript. All authors read and approved the final manuscript.”
“Background Cell proliferation, that represents the essence of cancer disease, involves not only a deregulated control of cell cycle but also adjustments of energy metabolism PSI-7977 in order to fuel cell growth and division. In fact, proliferation of cancer cells is accompanied by glycolysis activation and this altered glucose metabolism is one of the most common hallmark of cancer

[1, 2]. Approximately 60 to 90% of cancers display a metabolic profile, the so-called Warburg phenotype, characterized by their dependence upon glycolysis as the major source of energy, irrespective of the oxygen level [3]. According to the Warburg effect, cancer cells up-regulate glucose transporters, notably GLUT-1, and convert pyruvate, the end-product of glycolysis, into lactate by lactate dehydrogenase (LDH), rather than oxidizing it in mitochondria [4–6]. In this context, the hypoxia inducible factor 1 (HIF-1) has been shown to play a fundamental role [7, 8]. HIF-1 is a transcription factor that consists of Sapanisertib an O2-regulated HIF-1α and a constitutively Carbachol expressed HIF-1β subunit. In cancer cells, HIF-1α is up-regulated and, in turn, activates the expression of glycolytic enzymes (such as LDH) and glucose transporters (such as GLUT-1), and down-regulates the mitochondrial activity through several mechanisms, in particular by inhibiting the conversion of pyruvate to acetyl-CoA via the activation

of the gene encoding pyruvate dehydrogenase kinase 1 [7–10]. Shifting metabolism away from mitochondria (glucose oxidation) and towards the cytoplasm (glycolysis) might suppress apoptosis, a form of cell death that is dependent on mitochondrial energy production [11, 12]. Accordingly, the glycolytic phenotype has been associated to apoptosis resistance and consequently Metabolism inhibitor increased tumor cell proliferation [3, 4, 13]. Understanding the metabolic basis of cancer has the potential to provide the foundation for the development of novel approaches targeting tumor metabolism [14]. In this regard, recent observations suggest that the reversion of the glycolytic phenotype may render tumor cells susceptible to apoptosis and decrease their growth rate [15–17]. With this in mind, we planned to investigate whether the natural supplement Cellfood™ (CF; Nu Science Corporation, CA, USA) might have antiproliferative effects in vitro, limiting cell proliferation and promoting cell death.