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| Fructose-1,6-bisphosphatase (FBPase) is a key enzyme of gluconeogenesis that has garnered significant attention in cancer research. Altered metabolic pathways are hallmarks of cancer, and many tumors rely on aerobic glycolysis (the Warburg effect) rather than oxidative phosphorylation even in the presence of oxygen. In this context, the expression and activity of FBPase—primarily FBP1 and to some extent FBP2—play important roles in modulating cancer metabolism as well as impacting patient prognosis. FBP1 (Fructose-1,6-Bisphosphatase 1) is a key enzyme in gluconeogenesis, the process by which cells generate glucose from non-carbohydrate sources. FBP1 is often downregulated in cancer cells, and its low expression is associated with poor prognosis. FBP1 is a key enzyme in the regulation of the Warburg effect, a metabolic phenomenon in which cancer cells preferentially use glycolysis for energy production, even in the presence of oxygen. FBP1 activators are being developed as a potential therapeutic strategy for cancer treatment. Key Role in Gluconeogenesis -FBPase catalyzes the conversion of fructose-1,6-bisphosphate to fructose-6-phosphate, which is a pivotal step in gluconeogenesis. -This counteracts glycolysis—a pathway often upregulated in cancer cells to support rapid proliferation and biomass generation. Altered FBPase Expression in Cancer -A decrease or loss of FBP1 expression has been observed in several cancer types FBP1: -Primarily found in the liver and kidney. -Plays a central role in gluconeogenesis by catalyzing the conversion of fructose-1,6-bisphosphate to fructose-6-phosphate. -Its expression is more frequently linked to altered metabolic states in various cancers (e.g., reduced FBP1 is often associated with a glycolytic and more aggressive tumor metabolism). FBP2: -Known as the muscle isoform of fructose-1,6-bisphosphatase. -While it performs a similar catalytic function, its expression profile and regulation differ from FBP1 and it is less commonly associated with the metabolic rewiring observed in many cancers. |
| Cyclooxygenase (COX)-2 overexpression has been noted in various cancers.
PI3Ks/AKT pathways are over-activated in several types of cancers. EGFR altered activity has been noted in various pathological conditions. However, its regulation is an important step in the inhibition of cancer. In this regard, EGCG shows a pivotal role in the inhibition of EGFR activity. Activating protein-1 transcription factor has been associated with pathogenesis including cancer. Activation of the sonic hedgehog (Shh) pathway is required for the growth of numerous tissues and organs and recent evidence indicates that this pathway is often recruited to stimulate growth of cancer stem cells (CSCs) and to orchestrate the reprogramming of cancer cells via epithelial mesenchymal transition (EMT). Increased expression of Nanog has been associated with the aggressive nature of certain cancers, highlighting its role in promoting cancer stem cell characteristics. The aberrant hedgehog (Hh)/GLI signaling pathway causes the formation and progression of a variety of tumors. The process of cell apoptosis is often accompanied by the destruction of mitochondrial transmembrane potential, which is widely regarded as one of the earliest events in the process of cell apoptosis. Human malignancies frequently exhibit mutations in the TGF-β pathway, and overactivation of this system is linked to tumor growth by promoting angiogenesis and inhibiting the innate and adaptive antitumor immune responses50. Several studies have demonstrated that high cyclin D1 expression was observed in cancers including breast, lung, prostate, lymph node and colorectal cancers [23–25]. The oncogene c-myc, which is frequently over-expressed in cancer cells, is involved in the transactivation of most of the glycolytic enzymes including lactate dehydrogenase A (LDHA) and the glucose transporter GLUT1 [51,52]. Thus, c-myc activation is a likely candidate to promote the enhanced glucose uptake and lactate release in the proliferating cancer cell. Vimentin is overexpressed in various epithelial cancers, including prostate cancer, gastrointestinal tumors, tumors of the central nervous system, breast cancer, malignant melanoma, and lung cancer. Vimentin’s overexpression in cancer correlates well with accelerated tumor growth, invasion, and poor prognosis; however, the role of vimentin in cancer progression remains obscure. Heat shock proteins (HSPs) are normally induced under environmental stress to serve as chaperones for maintenance of correct protein folding but they are often overexpressed in many cancers, including breast cancer. Since NQO1 is highly expressed in many solid tumors, including via upregulation of Nrf2, the design of compounds activated by NQO1 and NQO1-targeted drug delivery have been active areas of research. Since increased Nrf2 gene expression is one of the main mechanisms of cancer cells in resisting chemotherapeutic drugs and survival in oxidative conditions; finding compounds with the ability to suppress Nrf2 gene expression with minimum side effects can be considered an important strategy for increasing the sensitivity of cancer cells to chemotherapy. Overexpression of c-met stimulates proliferation, migration and invasion in various types of cancer including prostate cancer. Overexpression of TGFα and EGFR by many carcinomas correlates with the development of cancer metastasis, resistance to chemotherapy and poor prognosis. More than 50% of human cancers have a mutated nonfunctional p53. |
| 1578- | Citrate, | Understanding the Central Role of Citrate in the Metabolism of Cancer Cells and Tumors: An Update |
| - | Review, | Var, | NA |
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