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dc.contributor.authorSterea, Andra Mihaela
dc.date.accessioned2018-09-04T11:44:08Z
dc.date.available2018-09-04T11:44:08Z
dc.date.issued2018-09-04T11:44:08Z
dc.identifier.urihttp://hdl.handle.net/10222/74200
dc.description.abstractProstate cancer (PCa) represents a multifactorial and complex disease affecting thousands of men each year. Although the prognosis of PCa is improving, limitations in early diagnosis pose a challenge for the effective treatment of patients with late stages of the disease. Research is now focusing on targeting ion channels as a means of delaying the progression of PCa in patients who do not respond to traditional therapies. One potential target is the ion channel TRPML1 whose function mediates cellular bioenergetics. Here, we demonstrate that TRPML1 is overexpressed in PCa cells and its downregulation decreases cell proliferation. At the molecular level, the loss of TRPML1 impairs autophagy resulting in the accumulation of free radicals, ultimately leading to DNA damage and cell cycle arrest. Our data suggests an important role for TRPML1 in the maintenance of PCa cell proliferation and its potential as a novel therapeutic target for the treatment of PCa.en_US
dc.language.isoenen_US
dc.subjectProstate Canceren_US
dc.subjectTRPML1en_US
dc.subjectTargeted therapyen_US
dc.subjectLysosomesen_US
dc.subjectAutophagyen_US
dc.subjectIon channelsen_US
dc.titleTRPML1 REGULATES PROSTATE CANCER CELL PROLIFERATION THROUGH THE MODULATION OF OXIDATIVE STRESS AND CELL CYCLEen_US
dc.date.defence2018-08-16
dc.contributor.departmentDepartment of Physiology & Biophysicsen_US
dc.contributor.degreeMaster of Scienceen_US
dc.contributor.external-examinerCatherine Tooen_US
dc.contributor.graduate-coordinatorAlexander Quinnen_US
dc.contributor.thesis-readerElizabeth Cowleyen_US
dc.contributor.thesis-readerZhenyu Chengen_US
dc.contributor.thesis-readerValerie Chappeen_US
dc.contributor.thesis-supervisorYassine El Hianien_US
dc.contributor.ethics-approvalNot Applicableen_US
dc.contributor.manuscriptsNot Applicableen_US
dc.contributor.copyright-releaseNot Applicableen_US
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