LSM1 AND RNY1: CLUES IN THE SEARCH FOR HOW RNA METABOLIC PATHWAYS CONTROL CANCER

Persistent Link:
http://hdl.handle.net/10150/204114
Title:
LSM1 AND RNY1: CLUES IN THE SEARCH FOR HOW RNA METABOLIC PATHWAYS CONTROL CANCER
Author:
Luhtala, Natalie
Issue Date:
2011
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.
Embargo:
Embargo: Release after 4/7/2012
Abstract:
Carcinogenesis requires numerous alterations to gene expression to evade normal controls on cellular growth, invasion, and immortality. Traditionally, these changes have been examined in the context of deregulated transcriptional control of oncogenes and tumor suppressors. However, in recent years, research has revealed that processes outside of transcription such as RNA splicing, translation, and decay are also deregulated in cancers, sustaining tumorigenic potential. This dissertation details our investigation into the cellular functions of two RNA metabolic proteins whose human orthologs are deregulated in tumors: a putative oncogene, Lsm1, and a putative tumor suppressor, Rny1. Herein, we reveal interesting functions for these proteins that might provide insight into their roles in carcinogenesis. First, we demonstrate a role for Lsm1 over-expression in altered splicing through depletion of U6 snRNA levels. Second, we clarify the mechanism for Rny1's activity against RNA substrates and identify cis regions required for its non-catalytic role in growth inhibition. Overall, this knowledge expands our understanding of how RNA metabolism might be deregulated in cancer and could provide novel pathways to target for synthetic lethal responses in cancers with altered expression of these proteins.
Type:
text; Electronic Dissertation
Degree Name:
Ph.D.
Degree Level:
doctoral
Degree Program:
Graduate College; Cancer Biology
Degree Grantor:
University of Arizona
Advisor:
Parker, Roy

Full metadata record

DC FieldValue Language
dc.language.isoenen_US
dc.titleLSM1 AND RNY1: CLUES IN THE SEARCH FOR HOW RNA METABOLIC PATHWAYS CONTROL CANCERen_US
dc.creatorLuhtala, Natalieen_US
dc.contributor.authorLuhtala, Natalieen_US
dc.date.issued2011-
dc.publisherThe University of Arizona.en_US
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_US
dc.description.releaseEmbargo: Release after 4/7/2012en_US
dc.description.abstractCarcinogenesis requires numerous alterations to gene expression to evade normal controls on cellular growth, invasion, and immortality. Traditionally, these changes have been examined in the context of deregulated transcriptional control of oncogenes and tumor suppressors. However, in recent years, research has revealed that processes outside of transcription such as RNA splicing, translation, and decay are also deregulated in cancers, sustaining tumorigenic potential. This dissertation details our investigation into the cellular functions of two RNA metabolic proteins whose human orthologs are deregulated in tumors: a putative oncogene, Lsm1, and a putative tumor suppressor, Rny1. Herein, we reveal interesting functions for these proteins that might provide insight into their roles in carcinogenesis. First, we demonstrate a role for Lsm1 over-expression in altered splicing through depletion of U6 snRNA levels. Second, we clarify the mechanism for Rny1's activity against RNA substrates and identify cis regions required for its non-catalytic role in growth inhibition. Overall, this knowledge expands our understanding of how RNA metabolism might be deregulated in cancer and could provide novel pathways to target for synthetic lethal responses in cancers with altered expression of these proteins.en_US
dc.typetexten_US
dc.typeElectronic Dissertationen_US
thesis.degree.namePh.D.en_US
thesis.degree.leveldoctoralen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.disciplineCancer Biologyen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.contributor.advisorParker, Royen_US
dc.contributor.committeememberBriehl, Margareten_US
dc.contributor.committeememberGerner, Eugeneen_US
dc.contributor.committeememberHurley, Laurenceen_US
dc.contributor.committeememberWeinert, Teden_US
dc.identifier.proquest11464-
dc.identifier.oclc752261332-
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