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Therapeutic Targeting of Cancer Cell Metabolism : Role of Metabolic Enzymes , Oncogenes and Tumor Suppressor Genes
| Content Provider | Semantic Scholar |
|---|---|
| Author | Majeed, Rabiya Hamid, Abid Qurishi, Yasrib Qazi, Asif Khurshid Hussain, Aashiq Ahmed, Mudassier Najar, Rauf Ahmad Bhat, Javeed Ahmad Singh, Shashank Kumar Saxena, Ajit Kumar |
| Copyright Year | 2012 |
| Abstract | The metabolic response in mammalian cells requires a coordination of cellular activities that include cell proliferation with nutrient availability, regulation of energy homeostasis and hormonal and stress signaling. Cancer cells require unrestricted energy generation from ATP for their uncontrolled proliferation. Over the last few decades, there are accumulating evidences about the metabolic reorganization during cancer development which has been obtained from studies on various tumor types. The involvement of various metabolic enzymes and oncogenic proteins to cancer progression widen beyond the control of cell growth and division, and these may be responsible for the metabolic alterations associated to the pathogenesis of human cancers. It is well acknowledged that accessibility of nutrient enables nucleic acid, protein and lipid biosynthesis which helps to promote cell proliferation that is again associated with increased glycolytic flux and decreased oxidative metabolism. This transition to glycolysis for energy production provides several advantages to the tumor including adaptation to a low oxygen environment and the acidification of the surrounding microenvironment, which promotes tumor invasion and suppresses immune surveillance and the most important it provides necessary precursors for other biochemical pathways [1]. In contrast, lack of nutrient availability triggers a metabolic switch that leads to hyper activation of energy producing pathways, such as oxidative phosphorylation that restrict cell proliferation. In non-proliferating cells catabolic system is predominantly used to fulfill the energy requirements which use the mitochondrial oxidative phosphorylation along with oxidation of macromolecules to accomplish the energy needs. However, in highly proliferating tissues with high glycolytic flux, biosynthesis of macromolecules and lactate production leads to cell cycle progression, leading to a shift toward an anabolic metabolism [2]. Therefore metabolism and cell proliferation are under the common regulatory pathway to ensure a coordinated cellular response. Several pathophysiological conditions are associated with flux to a glycolytic metabolism and now it is an established fact that cancer progression and invasiveness is associated with major metabolic alterations. So the similar factors that trigger proliferation, e.g. oncogenes and some metabolic enzymes, the same factors coordinate the metabolic response of the cells to the external stimuli. |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | https://www.omicsonline.org/therapeutic-targeting-of-cancer-cell-metabolism-role-of-metabolic-enzymes-oncogenes-and-tumor-suppressor-genes-1948-5956.1000156.pdf |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | Accessibility Acclimatization Anabolic steroids Anabolism Automated theorem proving Biomarkers, Tumor Body tissue Cell Cycle Progression Cell Nucleus Cell Proliferation Cell Respiration Cellular Phone Color gradient Cross Reactions Crosstalk Gene regulatory network Glycolysis Habitat Hope (emotion) Hyperactive behavior Immunologic Surveillance Lactic acid Leukemia, B-Cell Lipogenesis Metabolic Process, Cellular Neoplasms Nephroblastoma Nucleic Acids Oncogenes Oxidative Phosphorylation Oxygen Precipitating Factors Requirement Suppressor Factors, Immunologic Tumor Progression Uncontrolled format string cell growth energy homeostasis macromolecule oxidation |
| Content Type | Text |
| Resource Type | Article |
