An Attempt to Reverse Aspects of the Warburg Effect Using 17 β-estradiol

Nelson, Vanessa

dc.contributor.author	Nelson, Vanessa
dc.date.accessioned	2012-05-01T14:50:01Z
dc.date.available	2012-05-01T14:50:01Z
dc.date.issued	2012-05-01
dc.identifier.uri	http://hdl.handle.net/10150/221348
dc.description	A Thesis submitted to The University of Arizona College of Medicine - Phoenix in partial fulfillment of the requirements for the Degree of Doctor of Medicine.	en
dc.description.abstract	The Warburg effect is defined as the propensity for cancer cells to favor glycolysis over oxidative phosphorylation under aerobic conditions. Finding a way to reverse this effect would likely be very beneficial for cancer therapy. The PI3K/Akt pathway has been suggested to be responsible for the Warburg effect, and estrogen is a known regulator of this pathway. Estrogen, specifically 17 β-estradiol, has been shown to be protective at the level of the mitochondria. The purpose of this study was to try to use 17 β-estradiol to reverse aspects of the Warburg effect in two cancer lines. Various concentrations of 17 β-estradiol were added to the samples (0, 10nm, 100nm, 1μm) for various amounts of time (16-96h). Western blots probes for select subunits of the electron transport chain (ETC) showed no differences in cells with and without 17 β-estradiol across various times. Due to technical difficulties with cell lines, considerable troubleshooting was required, consuming the time available for further analysis. The available results do not suggest that 17 β-estradiol alone is able to reverse the Warburg effect.
dc.language.iso	en_US	en
dc.publisher	The University of Arizona.	en_US
dc.rights	Copyright © is held by the author. Digital access to this material is made possible by the College of Medicine - Phoenix, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.	en_US
dc.subject	Warburg Effect	en
dc.subject.mesh	Estradiol	en
dc.title	An Attempt to Reverse Aspects of the Warburg Effect Using 17 β-estradiol	en_US
dc.type	text; Electronic Thesis	en
dc.contributor.department	The University of Arizona College of Medicine - Phoenix	en
dc.description.collectioninformation	This item is part of the College of Medicine - Phoenix Scholarly Projects 2012 collection. For more information, contact the Phoenix Biomedical Campus Library at pbc-library@email.arizona.edu.	en_US
dc.contributor.mentor	Valla, Jon	en
refterms.dateFOA	2018-06-26T07:55:18Z
html.description.abstract	The Warburg effect is defined as the propensity for cancer cells to favor glycolysis over oxidative phosphorylation under aerobic conditions. Finding a way to reverse this effect would likely be very beneficial for cancer therapy. The PI3K/Akt pathway has been suggested to be responsible for the Warburg effect, and estrogen is a known regulator of this pathway. Estrogen, specifically 17 β-estradiol, has been shown to be protective at the level of the mitochondria. The purpose of this study was to try to use 17 β-estradiol to reverse aspects of the Warburg effect in two cancer lines. Various concentrations of 17 β-estradiol were added to the samples (0, 10nm, 100nm, 1μm) for various amounts of time (16-96h). Western blots probes for select subunits of the electron transport chain (ETC) showed no differences in cells with and without 17 β-estradiol across various times. Due to technical difficulties with cell lines, considerable troubleshooting was required, consuming the time available for further analysis. The available results do not suggest that 17 β-estradiol alone is able to reverse the Warburg effect.