| Grant number: | 15/25832-4 |
| Support Opportunities: | Regular Research Grants |
| Start date: | November 01, 2016 |
| End date: | April 30, 2019 |
| Field of knowledge: | Biological Sciences - Biochemistry - Chemistry of Macromolecules |
| Principal Investigator: | Sandra Martha Gomes Dias |
| Grantee: | Sandra Martha Gomes Dias |
| Host Institution: | Centro Nacional de Pesquisa em Energia e Materiais (CNPEM). Campinas , SP, Brazil |
| City of the host institution: | Campinas |
| Associated researchers: | Andre Luis Berteli Ambrosio |
Abstract
Molecular mechanisms related to the tumorigenic process are traditionally related to oncogenes and tumor supressors deregulation, which control the signaling pathways responsible for the cell cycle regulation, cell growth, cell proliferation and cell death. On the other hand, new evidences point to an alternative mechanism where the primary role of the oncogenes and tumor supressors are to reprogram the cellular metabolism. This scenario is consistent with the recent discoveries that some metabolites can be oncogenic by itself, altering cell signaling and blocking cell differentiation. Such metabolic signals act by determining chromatin structure, since they are substrates for the enzymes involved on chromatin remodeling through histone and DNA modification. Changes on both actions will define epigenetic remodeling and genic transcriptional control. On this project, we will study how the glutamine metabolism into ±-ketoglutarate, specifically related to the glutaminases, affect chromatin remodeling and epigenetic control of pathways important for the cancer stem cell (CSC) phenotype maintenance. Although not very much appreciated, metabolic and nutrient signaling (either direct or intermediated by enzymes) also perform an important role on gene trancriptional control by altering the activity of several transcriptional factors. On this project, we will also evolve the findings made by our lab that the HIF (Hypoxia-inducible factor)-3± isoform directly interacts with lipids, by pursuing the understanding of how this interaction can affect this isoform activity; in addition, we want to describe the molecular and functional details of a protein-protein interaction discovered in our lab, involving the glutaminase and the nuclear receptor PPAR³. (AU)
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