Show simple item record

dc.contributor.advisorHurley, Laurenceen
dc.contributor.authorNeeb, Megan Ann
dc.creatorNeeb, Megan Annen
dc.date.accessioned2015-10-05T22:19:10Zen
dc.date.available2015-10-05T22:19:10Zen
dc.date.issued2015en
dc.identifier.citationNeeb, Megan Ann. (2015). MYC Inhibition Through Small Compound Targeting of the NHE III₁ i-Motif (Bachelor's thesis, University of Arizona, Tucson, USA).
dc.identifier.urihttp://hdl.handle.net/10150/579322en
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.
dc.language.isoen_USen
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.rights.urihttp://rightsstatements.org/vocab/InC/1.0/
dc.titleMYC Inhibition Through Small Compound Targeting of the NHE III₁ i-Motifen_US
dc.typetexten
dc.typeElectronic Thesisen
thesis.degree.grantorUniversity of Arizonaen
thesis.degree.levelbachelorsen
thesis.degree.disciplineHonors Collegeen
thesis.degree.disciplineBiochemistryen
thesis.degree.nameB.S.en
refterms.dateFOA2018-08-13T17:56:30Z
html.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.


Files in this item

Thumbnail
Name:
azu_etd_mr_2015_0203_sip1_m.pdf
Size:
1.408Mb
Format:
PDF

This item appears in the following Collection(s)

Show simple item record