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. / 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.
| Identifer | oai:union.ndltd.org:arizona.edu/oai:arizona.openrepository.com:10150/221348 |
| Date | 01 May 2012 |
| Creators | Nelson, Vanessa |
| Contributors | The University of Arizona College of Medicine - Phoenix, Valla, Jon, PhD |
| Publisher | The University of Arizona. |
| Source Sets | University of Arizona |
| Language | en_US |
| Detected Language | English |
| Type | Thesis |
| 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. |
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