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Title page for ETD etd-07172015-083313


Type of Document Dissertation
Author Guyer, Richard Allen
URN etd-07172015-083313
Title Tumor suppressor mechanisms of the polarity protein Par3
Degree PhD
Department Cell and Developmental Biology
Advisory Committee
Advisor Name Title
Ethan Lee Committee Chair
Andrea Page-McCaw Committee Member
Ian Macara Committee Member
Jennifer Pietenpol Committee Member
Matthew Tyska Committee Member
Keywords
  • aPKC
  • polarity
  • Par3
  • Stat3
Date of Defense 2014-10-23
Availability unrestricted
Abstract
Proteins that regulate cell polarity are fundamental for metazoan biology and are necessary for proper development of tissues and organs. In light of polarity genes’ fundamental role in tissue organization, disruptions in polarity networks have been suspected to promote neoplasia. Studies in Drosophila melanogaster models and correlative data from human tumor samples have supported this hypothesis, but direct experimental support for polarity genes as mammalian tumor suppressors has only recently been reported. The polarity regulator Par3 has emerged as a suppressor of growth and metastasis in mammary and skin tumors. The mechanisms by which Par3 restrains tumor progression, however, remain obscure. In the studies reported here, I show that loss of Par3 can promote activation of an oncogenic signaling pathway in mouse mammary cells by permitting aPKCι/λ to activate NF-κB signaling. These studies demonstrate that preventing aberrant aPKC activity is a key tumor suppressor function of Par3. This mechanism may be relevant to human tumors.
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