Oncogene Ras and Mitochondrial activity
| Author: | L. Alberghina |
|---|---|
| Submitted: | Thursday 10th of February 2011 10:11:04 AM |
| Submitted by: | egf |
| Language: | English |
| Content type: | Learning resource |
| Educational levels: | expert, qc3 |
Contents
Topics
- Genetics + genomics
- Clinical/medical genetics
- Clinical/medical genetics > Disease related (typology of disorder)
- Clinical/medical genetics > Disease related (typology of disorder) > Cancer genetics
- Clinical/medical genetics > Disease related (typology of disorder) > Cancer genetics > Growth regulation
- Clinical/medical genetics > Disease related (typology of disorder) > Cancer genetics > Growth regulation > Oncogenes
- Clinical/medical genetics > Patient related
- Clinical/medical genetics > Patient related > Patient/family related
- Clinical/medical genetics > Patient related > Patient/family related > Patient management
- Clinical/medical genetics > Patient related > Patient/family related > Patient management > Diagnosis of patient disease
- Clinical/medical genetics > Patient related > Patient/family related > Patient management > Diagnosis of patient disease > Laboratory investigation
- Clinical/medical genetics > Patient related > Patient/family related > Patient management > Diagnosis of patient disease > Laboratory investigation > Biochemical (clinical investigation)
- Molecular genetics
- Molecular genetics > Studies of RNA
- Molecular genetics > Studies of RNA > Studies of coding RNA
- Molecular genetics > Studies of RNA > Studies of coding RNA > Studies of protein
- Molecular genetics > Studies of DNA
- Molecular genetics > Studies of DNA > Mitochondrial DNA
Abstract
Complex cellular functions are often determined by the dynamic interactions occurring in networks of hundreds or thousands gene products that generate system-level properties largely unpredictable considering only the behaviour of individual nodes of the network. The phenotype of “in vitro” growing cancer cells is thus going to be considered as an integration of system-level properties, whose underlying network are analyzed by genome-wide and hypothesis driven experiments under various nutrients perturbations. The following results have been obtained: low glucose reduces proliferation of transformed cells and enhances their death; low glutamine reduces proliferation of transformed cells and arrest them in S phase; signalling pathways relevant for cell proliferation are differentially affected by nutrient perturbations in normal and transformed cells; transformed cells as compared to normal ones present: enhanced glycolysis; increased mitochondrial potential; altered mitochondrial fusion/fission; reduced amounts and activity of mitochondrial Complex I; cAMP/PKA pathway is down-regulated in many cancer cell lines; stimulation of PKA pathway by forskolin slightly inhibits normal cell proliferation, protects transformed cells from low glucose induced cell death, enhances mitochondrial activity and stimulates Complex I activity and expression; metabolome analysis performed with stable isotope labelling of glucose and glutamine indicate that transformed cells undergo metabolic remodelling that involves glycolysis and mitochondrial metabolism of glucose and glutamine derived products. The above findings are discussed in a systems biology approach.
alberghina_5121.pdf
Citation
L. Alberghina. Oncogene Ras and Mitochondrial activity. EUROGENE portal. February 2011. online: http://eurogene.open.ac.uk/content/oncogene-ras-and-mitochondrial-activity
Keywords
adenosine triphosphate, apoptosis, bioinformatics, biotechnology, cancer genetics, cell, cell cycle, cell line, dominant, electrophoresis, expression, fibroblast, gene, gene expression, gene product, genetics, genome, in vitro, isolated, metabolism, mitochondria, mutant, nucleotide, oncogene, oncogenic, phase, phenotype, probe, protein, recessive, replication, screening, synthesis, transcription, transformation, vectorTerms of use
This work is licensed under a Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported License. Read more.