Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/119879
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dc.titleA ROLE OF PRL-3 IN AUTOPHAGY AND ITS REGULATION IN HUMAN CANCERS
dc.contributor.authorHUANG YUHAN
dc.date.accessioned2015-06-09T18:00:15Z
dc.date.available2015-06-09T18:00:15Z
dc.date.issued2015-01-23
dc.identifier.citationHUANG YUHAN (2015-01-23). A ROLE OF PRL-3 IN AUTOPHAGY AND ITS REGULATION IN HUMAN CANCERS. ScholarBank@NUS Repository.
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/119879
dc.description.abstractPRL-3 (PTP4A3) IS A PHOSPHATASE THAT PROMOTES MULTIPLE ONCOGENIC PROCESSES. RECENTLY, WE FOUND THE CORRELATION OF PRL-3 AND AUTOPHAGY. AUTOPHAGY IS A ?SELF-EATING? PROCESS WHICH HAS DUAL ROLES IN PROMOTING OR SUPPRESSING TUMOR GROWTH, DEPENDING ON CELLULAR CONTEXT. IN THIS STUDY, I SHOWED PRL-3 OVEREXPRESSION ENHANCES HVPS34-BECLIN-1-DEPENDENT AUTOPHAGOSOME FORMATION, AND ACCELERATES ATG5 DEPENDENT LC3 CONVERSION. PRL-3 OVEREXPRESSION ALSO ACCELERATES THE DEGRADATION OF SQSTM/P62, WHICH IS A KNOWN AUTOPHAGY SUBSTRATE. SURPRISINGLY, PRL-3 ITSELF IS ALSO DEGRADED BY AUTOPHAGY, FORMING A NEGATIVE FEEDBACK LOOP WITH AUTOPHAGY. CLINICALLY, PRL-3 IS DEPENDENT ON AUTOPHAGY ACTIVITY IN PROMOTING OVARIAN CANCER PROGRESSION. IN ADDITION, I SHOWED THAT CONSTITUTIVELY ACTIVATED MUTATION OF KRAS, WHICH IS ESSENTIAL IN THE DEVELOPMENT OF MANY HUMAN CANCERS, SPECIFICALLY UPREGULATED PRL-3 PROTEIN LEVEL. MY STUDY SHOWED NEW MECHANISMS OF PRL-3 REGULATIONS AS WELL AS THE PATHWAYS AFFECTED BY PRL-3, WHI
dc.language.isoen
dc.subjectPRL-3, post-transcriptional regulation, autophagy, cancer, prognosis, KRas mutation
dc.typeThesis
dc.contributor.departmentNUS GRAD SCH FOR INTEGRATIVE SCI & ENGG
dc.contributor.supervisorTHIERY JEAN PAUL
dc.contributor.supervisorZENG QI
dc.description.degreePh.D
dc.description.degreeconferredDOCTOR OF PHILOSOPHY
dc.identifier.isiutNOT_IN_WOS
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