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https://scholarbank.nus.edu.sg/handle/10635/121847
DC Field | Value | |
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dc.title | THE MECHANISM OF PRL-3 SIGNALLING UNDER CELLULAR STRESS | |
dc.contributor.author | YE ZU | |
dc.date.accessioned | 2015-12-10T18:00:20Z | |
dc.date.available | 2015-12-10T18:00:20Z | |
dc.date.issued | 2015-08-20 | |
dc.identifier.citation | YE ZU (2015-08-20). THE MECHANISM OF PRL-3 SIGNALLING UNDER CELLULAR STRESS. ScholarBank@NUS Repository. | |
dc.identifier.uri | http://scholarbank.nus.edu.sg/handle/10635/121847 | |
dc.description.abstract | PRL-3 IS KNOWN TO EXHIBIT PLEIOTROPIC EFFECTS IN CANCER PROGRESSION, INCLUDING PROMOTING CELL PROLIFERATION, SUSTAINING CELL SURVIVAL, INDUCING ANGIOGENESIS, AND ENHANCING INVASION AND METASTASIS. HOWEVER, THE SIGNALLING MECHANISMS OF PRL-3 REMAIN LARGELY UNKNOWN. HERE, PRL-3 WAS IDENTIFIED AS A NOVEL ACTIVATOR OF MTORC1. PRL-3 INDUCED AN ABERRANT ACTIVATION OF MTOR SIGNALLING IN CANCER CELLS BY USING A TWO-PRONGED APPROACH: 1) INCREASING RHEB-GTP ACCUMULATION VIA ACTIVATION OF AKT-TSC2 SIGNALLING, AND 2) ENHANCING RAG GTPASES-MEDIATED MTORC1 RECRUITMENT TO LYSOSOMES FOR RHEB-MEDIATED ACTIVATION. THIS PRL-3-MEDIATED ACTIVATION OF MTORC1 RESULTED IN INCREASED CELL MOTILITY, INVASIVENESS, AND MMP-2/9 PRODUCTION. MOREOVER, A PROTECTIVE EFFECT OF PRL-3 AGAINST COCL2-INDUCED APOPTOSIS WAS REPORTED. THIS WAS P38 MAPK-DEPENDENT AND MECHANISTICALLY INVOLVED DEPHOSPHORYLATION OF THE PRO-APOPTOTIC KINASE. THESE FINDINGS CONTRIBUTE TO OUR UNDERSTANDING OF PRL-3 SIGNALLING AND HIGHLIGHT POTENTIAL | |
dc.language.iso | en | |
dc.subject | PRL-3, mTOR, p38 MAPK, cancer, stress, anti-apoptosis | |
dc.type | Thesis | |
dc.contributor.department | PHYSIOLOGY | |
dc.contributor.supervisor | SHEN HAN MING | |
dc.contributor.supervisor | ZENG QI | |
dc.description.degree | Ph.D | |
dc.description.degreeconferred | DOCTOR OF PHILOSOPHY | |
dc.identifier.isiut | NOT_IN_WOS | |
Appears in Collections: | Ph.D Theses (Open) |
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YEZU.pdf | 7.11 MB | Adobe PDF | OPEN | None | View/Download |
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