{"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":[],"committee_chairs":[],"committee_members":[],"year":2015,"date_issued":"2015-01-23","date_published":"2015-01-23","updated_at":"2026-07-24T03:30:47Z","subjects":["PRL-3, post-transcriptional regulation, autophagy, cancer, prognosis, KRas mutation"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":null,"outbound_label":null,"outbound_source":null},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["HUANG YUHAN"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"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":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["https://scholarbank.nus.edu.sg/bitstreams/cf3b7068-2e03-418a-b552-3a5d3b13c88a/download"]}]},{"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. 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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. 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