Differential effect of glucose deprivation on MAPK activation in drug sensitive human breast carcinoma MCF-7 and multidrug resistant MCF-7/ADR cells
dc.contributor.author | Gupta, Anjali K. | en_US |
dc.contributor.author | Lee, Yong J. | en_US |
dc.contributor.author | Galoforo, Sandra S. | en_US |
dc.contributor.author | Berns, Christine M. | en_US |
dc.contributor.author | Martinez, Alvaro A. | en_US |
dc.contributor.author | Corry, Peter M. | en_US |
dc.contributor.author | Wu, Xiao-yu | en_US |
dc.contributor.author | Guan, Kun-Liang | en_US |
dc.date.accessioned | 2006-09-11T15:56:18Z | |
dc.date.available | 2006-09-11T15:56:18Z | |
dc.date.issued | 1997-05 | en_US |
dc.identifier.citation | Gupta, Anjali K.; Lee, Yong J.; Galoforo, Sandra S.; Berns, Christine M.; Martinez, Alvaro A.; Corry, Peter M.; Wu, Xiao-yu; Guan, Kun-Liang; (1997). "Differential effect of glucose deprivation on MAPK activation in drug sensitive human breast carcinoma MCF-7 and multidrug resistant MCF-7/ADR cells." Molecular and Cellular Biochemistry 170 (1-2): 23-30. <http://hdl.handle.net/2027.42/45332> | en_US |
dc.identifier.issn | 0300-8177 | en_US |
dc.identifier.issn | 1573-4919 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/45332 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=9144315&dopt=citation | en_US |
dc.description.abstract | We have investigated the effect of glucose deprivation treatment on the activation of mitogen activated protein kinases (MAPKs) in the drug-sensitive human breast carcinoma cells (MCF-7) and its drug resistant variant (MCF-7/ADR) cells. Western blots and in-gel kinase assays showed that glucose free medium was a strong stimulus for the activation of MAPK in MCF-7/ADR cells. No activation was seen in MCF-7 cells. MAPK was activated within 3 min of being in glucose free medium and it remained activated for over 1 h in MCF-7/ADR cells. After being returned to complete medium, 1 h was required for the MAPK to become deactivated. To investigate whether alternative sources of ATP could inhibit glucose deprivation induced MAPK activation, we added glutamine and glutamate to glucose deprived medium. The addition of glutamine did not reverse glucose deprivation induced MAPK activation in MCF-7/ADR cells. The addition of glutamate, however, decreased the MAPK activation and the length of time of activation. We observed an increase greater than three fold in MEK, Raf, Ras, and PKC activity with glucose deprivation in MCF-7/ADR cells. This suggests that glucose deprivation-induced MAPK activation is mediated through this signal transduction pathway. | en_US |
dc.format.extent | 71888 bytes | |
dc.format.extent | 3115 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Kluwer Academic Publishers; Springer Science+Business Media | en_US |
dc.subject.other | Cardiology | en_US |
dc.subject.other | Medical Biochemistry | en_US |
dc.subject.other | Oncology | en_US |
dc.subject.other | Glucose Deprivation | en_US |
dc.subject.other | MCF-7 | en_US |
dc.subject.other | Signal Transduction | en_US |
dc.subject.other | MAPK | en_US |
dc.subject.other | MCF-7/ADR | en_US |
dc.subject.other | Biochemistry, General | en_US |
dc.subject.other | Life Sciences | en_US |
dc.title | Differential effect of glucose deprivation on MAPK activation in drug sensitive human breast carcinoma MCF-7 and multidrug resistant MCF-7/ADR cells | en_US |
dc.type | Article | en_US |
dc.subject.hlbsecondlevel | Public Health | en_US |
dc.subject.hlbsecondlevel | Biological Chemistry | en_US |
dc.subject.hlbtoplevel | Science | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Biological Chemistry and Institute of Gerontology, University of Michigan Medical School, Ann Arbor, Michigan, 48109, USA | en_US |
dc.contributor.affiliationum | Department of Biological Chemistry and Institute of Gerontology, University of Michigan Medical School, Ann Arbor, Michigan, 48109, USA | en_US |
dc.contributor.affiliationother | Department of Radiation Oncology, Research Laboratories, William Beaumont Hospital, 3601 West Thirteen Mile Road, Royal Oak, Michigan, 48073, USA | en_US |
dc.contributor.affiliationother | Department of Radiation Oncology, Research Laboratories, William Beaumont Hospital, 3601 West Thirteen Mile Road, Royal Oak, Michigan, 48073, USA | en_US |
dc.contributor.affiliationother | Department of Radiation Oncology, Research Laboratories, William Beaumont Hospital, 3601 West Thirteen Mile Road, Royal Oak, Michigan, 48073, USA | en_US |
dc.contributor.affiliationother | Department of Radiation Oncology, Research Laboratories, William Beaumont Hospital, 3601 West Thirteen Mile Road, Royal Oak, Michigan, 48073, USA | en_US |
dc.contributor.affiliationother | Department of Radiation Oncology, Research Laboratories, William Beaumont Hospital, 3601 West Thirteen Mile Road, Royal Oak, Michigan, 48073, USA | en_US |
dc.contributor.affiliationother | Department of Radiation Oncology, Research Laboratories, William Beaumont Hospital, 3601 West Thirteen Mile Road, Royal Oak, Michigan, 48073, USA | en_US |
dc.contributor.affiliationumcampus | Ann Arbor | en_US |
dc.identifier.pmid | 9144315 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/45332/1/11010_2004_Article_127593.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1023/A:1006890316102 | en_US |
dc.identifier.source | Molecular and Cellular Biochemistry | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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