Signal transducer and activator of transcription-3 (STAT3) protein is a member of the STAT family of transcription factors which are initially located in the cytoplasm in their inactive form. STAT proteins are part of a group that is sometimes called DNA- binding factors. These proteins bind to DNA sequences, and therefore control the transcription of information from DNA to mRNA. A variety of growth factors and cytokines activate STAT3 by phosphorylating the tyrosine residue in the STAT3 transactivation domain. Phosphorylated STAT3 (p-STAT3) then translocates into the nucleus and induces the expression of a wide variety of target genes involved in tumorigenesis.
Tumor cells depend on STAT3 for continued rapid growth and avoidance of apoptosis. STAT3 is constitutively activated in a wide variety of tumours, including colorectal cancer, liver cancer, breast cancer, …
As discussed in our previous article, PFK1 (phosphofructokinase type 1) is a major regulatory enzyme in glycolysis.
Anti-tumor activity of Herbalzym Vinegar by disrupting cancer cell metabolism
PFK1 is an allosteric enzyme made of 4 subunits and controlled by many activators and inhibitors. PFK-1 catalyzes the important “committed” step of glycolysis, the conversion of fructose 6-phosphate and ATP to fructose 1,6-bisphosphate and ADP.
PFK1 is allosterically inhibited by high levels of ATP but AMP reverses the inhibitory action of ATP. Therefore, the activity of the enzyme increases when the cellular ATP/AMP ratio is lowered. Glycolysis is thus stimulated when energy charge falls. PFK1 has two sites with different affinities for …
The Warburg effect describes a pro-oncogenic metabolism switch such that cancer cells take up more glucose than normal tissue and favor incomplete oxidation of glucose even in the presence of oxygen. Most cancer cells exhibit increased glycolysis (the Warburg effect) and use this metabolic pathway for generation of ATP as a main source of their energy supply. A number of studies suggest several possible mechanisms by which this metabolic alteration may evolve during cancer development. These mechanisms include mitochondrial defects and malfunction, adaptation to hypoxic tumor microenvironment, oncogenic signaling, and abnormal expression of metabolic enzymes.
The glycolytic switch occupies a privileged position in the aggressive agenda of most solid tumors. As such, switching to a glycolytic metabolism may precede the evolution of tumors toward the more aggressive angiogenic and metastatic phenotypes. …
Cancer cells must satisfy the metabolic demands of fast-growing cancer within a continually changing microenvironment. The metabolism of cancer is approximately 8 times greater than that of normal cells and the body is constantly overworked trying to feed it. A fundamental difference in sugar metabolism exists between tumor cells found in the hypoxic regions of most solid tumors and the majority of normal cells in the body, which are under oxygen.
Sugar, or glucose, is brought into cells and converted into useable energy, a molecule called ATP. Another product of this conversion, a molecule called lactate, is then taken out of the cell by specialized transporters. Glucose is metabolized by glycolysis in a multi-step set of reactions resulting in the creation of pyruvate. In normal cells, much of this pyruvate …
