MYC Inhibition Through Small Compound Targeting of the NHE III₁ i-Motif

Persistent Link:
http://hdl.handle.net/10150/579322
Title:
MYC Inhibition Through Small Compound Targeting of the NHE III₁ i-Motif
Author:
Neeb, Megan Ann
Issue Date:
2015
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, 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.
Abstract:
Current cancer therapies often fail to eradicate a patient's tumors completely due to complications arising from protein mutations, tumor cell migration, and interference with DNA replication. These issues can be circumvented by inhibiting the oncogenes responsible for tumor growth through targeting of secondary non-helical structures present in the oncogenes' promoters. Through screening of NCI compound libraries we have found two compounds, IMC 30 and IMC 31, that are capable of reducing the expression of the oncogene MYC through interaction with the i-motif structure in its promoter region. These compounds are also capable of inducing cell death in cells that are reliant on MYC overexpression for growth. A third compound, IMC 16, was capable of inducing an increase in MYC expression in addition to inducing apoptosis in MYC dependent cells. This result indicates a possibility that increasing the expression of MYC in MYC dependent tumors may cause a shift in its primary function from cell growth to induction of apoptosis. The compounds IMC 30, IMC 31, and IMC 16 will be subjected to further experimentation with more complicated biological systems in an effort to develop them as cancer therapeutics.
Type:
text; Electronic Thesis
Degree Name:
B.S.
Degree Level:
bachelors
Degree Program:
Honors College; Biochemistry
Degree Grantor:
University of Arizona
Advisor:
Hurley, Laurence

Full metadata record

DC FieldValue Language
dc.language.isoen_USen
dc.titleMYC Inhibition Through Small Compound Targeting of the NHE III₁ i-Motifen_US
dc.creatorNeeb, Megan Annen
dc.contributor.authorNeeb, Megan Annen
dc.date.issued2015en
dc.publisherThe University of Arizona.en
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, 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
dc.description.abstractCurrent cancer therapies often fail to eradicate a patient's tumors completely due to complications arising from protein mutations, tumor cell migration, and interference with DNA replication. These issues can be circumvented by inhibiting the oncogenes responsible for tumor growth through targeting of secondary non-helical structures present in the oncogenes' promoters. Through screening of NCI compound libraries we have found two compounds, IMC 30 and IMC 31, that are capable of reducing the expression of the oncogene MYC through interaction with the i-motif structure in its promoter region. These compounds are also capable of inducing cell death in cells that are reliant on MYC overexpression for growth. A third compound, IMC 16, was capable of inducing an increase in MYC expression in addition to inducing apoptosis in MYC dependent cells. This result indicates a possibility that increasing the expression of MYC in MYC dependent tumors may cause a shift in its primary function from cell growth to induction of apoptosis. The compounds IMC 30, IMC 31, and IMC 16 will be subjected to further experimentation with more complicated biological systems in an effort to develop them as cancer therapeutics.en
dc.typetexten
dc.typeElectronic Thesisen
thesis.degree.nameB.S.en
thesis.degree.levelbachelorsen
thesis.degree.disciplineHonors Collegeen
thesis.degree.disciplineBiochemistryen
thesis.degree.grantorUniversity of Arizonaen
dc.contributor.advisorHurley, Laurenceen
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