{"id":{"repo_id":"nus","oai_identifier":"oai:scholarbank.nus.edu.sg:10635/119879"},"canonical_url":"https://search.dev.ndltd.org/etd/nus/oai:scholarbank.nus.edu.sg:10635/119879","repository":{"repo_id":"nus","name":"National University of Singapore","base_url":"https://scholarbank.nus.edu.sg/oai/request"},"display":{"title":"A ROLE OF PRL-3 IN AUTOPHAGY AND ITS REGULATION IN HUMAN CANCERS","abstract":"PRL-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","abstract_html":"PRL-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","abstract_has_math":false,"creators":["HUANG YUHAN"],"institution":null,"degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":["THIERY JEAN PAUL","ZENG QI"],"committee_chairs":[],"committee_members":[],"year":2015,"date_issued":"2015-01-23","date_published":"2015-01-23","updated_at":"2026-08-21T16:47:23Z","subjects":["PRL-3, post-transcriptional regulation, autophagy, cancer, prognosis, KRas mutation"],"languages":["en"],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://scholarbank.nus.edu.sg/handle/10635/119879","outbound_label":"Repository record","outbound_source":"dc:identifier.uri"},"source_record":{"url":"https://scholarbank.nus.edu.sg/oai/request?verb=GetRecord&metadataPrefix=dim&identifier=oai%3Ascholarbank.nus.edu.sg%3A10635%2F119879","prefix":"dim"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.other","label":"Dc Contributor Other","values":["NUS GRAD SCH FOR INTEGRATIVE SCI & ENGG"]},{"key":"dc:contributor.supervisor","label":"Supervisor","values":["THIERY JEAN PAUL","ZENG QI"]},{"key":"dc:creator","label":"Author","values":["HUANG YUHAN"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2015-06-09T18:00:15Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2015-06-09T18:00:15Z"]},{"key":"dc:date.issued","label":"Date","values":["2015-01-23"]},{"key":"dc:relation.isreferencedby","label":"Dc Relation Isreferencedby","values":["https://scholarbank.nus.edu.sg/handle/10635/119879"]},{"key":"dc:type","label":"Dc Type","values":["Thesis"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["PRL-3, post-transcriptional regulation, autophagy, cancer, prognosis, KRas mutation"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["en"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["https://scholarbank.nus.edu.sg/bitstreams/cf3b7068-2e03-418a-b552-3a5d3b13c88a/download","https://scholarbank.nus.edu.sg/handle/10635/119879"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["PRL-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"]},{"key":"dc:description.degree","label":"Dc Description Degree","values":["Ph.D"]},{"key":"dc:format.checksum.md5","label":"Dc Format Checksum Md5","values":["2ce6d67f2a80baed08952d2f7e23008a","420227e9865a5093ad104c4154793b74"]},{"key":"dc:title","label":"Title","values":["A ROLE OF PRL-3 IN AUTOPHAGY AND ITS REGULATION IN HUMAN CANCERS"]}]}],"canonical_facts":{"dc:contributor.other":["NUS GRAD SCH FOR INTEGRATIVE SCI & ENGG"],"dc:contributor.supervisor":["THIERY JEAN PAUL","ZENG QI"],"dc:creator":["HUANG YUHAN"],"dc:date.accessioned":["2015-06-09T18:00:15Z"],"dc:date.available":["2015-06-09T18:00:15Z"],"dc:date.issued":["2015-01-23"],"dc:description.abstract":["PRL-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:description.degree":["Ph.D"],"dc:format.checksum.md5":["2ce6d67f2a80baed08952d2f7e23008a","420227e9865a5093ad104c4154793b74"],"dc:identifier.uri":["https://scholarbank.nus.edu.sg/bitstreams/cf3b7068-2e03-418a-b552-3a5d3b13c88a/download","https://scholarbank.nus.edu.sg/handle/10635/119879"],"dc:language.iso":["en"],"dc:relation.isreferencedby":["https://scholarbank.nus.edu.sg/handle/10635/119879"],"dc:subject":["PRL-3, post-transcriptional regulation, autophagy, cancer, prognosis, KRas mutation"],"dc:title":["A ROLE OF PRL-3 IN AUTOPHAGY AND ITS REGULATION IN HUMAN CANCERS"],"dc:type":["Thesis"]},"updated_at":"2026-08-21T16:47:23Z"}