Ammonium ions improve the survival of glutamine-starved hybridoma cells. Issue 1 (December 2016)
- Record Type:
- Journal Article
- Title:
- Ammonium ions improve the survival of glutamine-starved hybridoma cells. Issue 1 (December 2016)
- Main Title:
- Ammonium ions improve the survival of glutamine-starved hybridoma cells
- Authors:
- Abusneina, Abdelmuhsen
Gauthier, Eric - Abstract:
- Abstract Background As a consequence of a reprogrammed metabolism, cancer cells are dependent on the amino acidl -glutamine for their survival, a phenomenon that currently forms the basis for the generation of new, cancer-specific therapies. In this paper, we report on the role which ammonium ions, a product of glutaminolysis, play on the survival ofl -glutamine-deprived Sp2/0-Ag14 mouse hybridoma cells. Results The supplementation ofl -glutamine-starved Sp2/0-Ag14 cell cultures with either ammonium acetate or ammonium chloride resulted in a significant increase in viability. This effect did not depend on the ability of cells to synthesizel -glutamine, and was not affected by the co-supplementation with α-ketoglutarate. When we examined the effect of ammonium acetate and ammonium chloride on the induction of apoptosis by glutamine deprivation, we found that ammonium salts did not prevent caspase-3 activation or cytochrome c leakage, indicating that they did not act by modulating core apoptotic processes. However, both ammonium acetate and ammonium chloride caused a significant reduction in the number ofl -glutamine-starved cells exhibiting apoptotic nuclear fragmentation and/or condensation. Conclusion All together, our results show that ammonium ions promote the survival ofl -glutamine-deprived Sp2/0-Ag14 cells and modulate late-apoptotic events. These findings highlight the complexity of the modulation of cell survival byl -glutamine, and suggest that targetingAbstract Background As a consequence of a reprogrammed metabolism, cancer cells are dependent on the amino acidl -glutamine for their survival, a phenomenon that currently forms the basis for the generation of new, cancer-specific therapies. In this paper, we report on the role which ammonium ions, a product of glutaminolysis, play on the survival ofl -glutamine-deprived Sp2/0-Ag14 mouse hybridoma cells. Results The supplementation ofl -glutamine-starved Sp2/0-Ag14 cell cultures with either ammonium acetate or ammonium chloride resulted in a significant increase in viability. This effect did not depend on the ability of cells to synthesizel -glutamine, and was not affected by the co-supplementation with α-ketoglutarate. When we examined the effect of ammonium acetate and ammonium chloride on the induction of apoptosis by glutamine deprivation, we found that ammonium salts did not prevent caspase-3 activation or cytochrome c leakage, indicating that they did not act by modulating core apoptotic processes. However, both ammonium acetate and ammonium chloride caused a significant reduction in the number ofl -glutamine-starved cells exhibiting apoptotic nuclear fragmentation and/or condensation. Conclusion All together, our results show that ammonium ions promote the survival ofl -glutamine-deprived Sp2/0-Ag14 cells and modulate late-apoptotic events. These findings highlight the complexity of the modulation of cell survival byl -glutamine, and suggest that targeting survival-signaling pathways modulated by ammonium ions should be examined as a potential anti-cancer strategy. … (more)
- Is Part Of:
- Cell & bioscience. Volume 6:Issue 1(2016)
- Journal:
- Cell & bioscience
- Issue:
- Volume 6:Issue 1(2016)
- Issue Display:
- Volume 6, Issue 1 (2016)
- Year:
- 2016
- Volume:
- 6
- Issue:
- 1
- Issue Sort Value:
- 2016-0006-0001-0000
- Page Start:
- 1
- Page End:
- 10
- Publication Date:
- 2016-12
- Subjects:
- Ammonium -- Apoptosis -- Caspase -- Glutamine -- Glutaminolysis -- Hybridoma
Biology -- Periodicals
Life sciences -- Periodicals
Cytology -- Periodicals
571.6 - Journal URLs:
- http://www.cellandbioscience.com/ ↗
http://www.ncbi.nlm.nih.gov/pmc/journals/1552/ ↗
http://link.springer.com/ ↗ - DOI:
- 10.1186/s13578-016-0092-8 ↗
- Languages:
- English
- ISSNs:
- 2045-3701
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - BLDSS-3PM
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- 10063.xml