Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/125944
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dc.titleARTESUNATE SUPPRESSES TUMOR GROWTH AND PROGRESSION OF PROSTRATE CANCER THROUGH THE MODULATION OF STAT3 AND NF-kB SIGNALING CASCADES
dc.contributor.authorALAMELU NACHIYAPPAN
dc.date.accessioned2016-07-13T18:00:14Z
dc.date.available2016-07-13T18:00:14Z
dc.date.issued2016-01-22
dc.identifier.citationALAMELU NACHIYAPPAN (2016-01-22). ARTESUNATE SUPPRESSES TUMOR GROWTH AND PROGRESSION OF PROSTRATE CANCER THROUGH THE MODULATION OF STAT3 AND NF-kB SIGNALING CASCADES. ScholarBank@NUS Repository.
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/125944
dc.description.abstractDRUG REPURPOSING, PROCESS OF IDENTIFYING NEW TARGETS FOR A CLINICALLY ACCEPTED DRUG THAT IS BEING USED FOR THE TREATMENT OF ANOTHER DISEASE, HAS GAINED A GREAT AMOUNT OF INTEREST IN THE FIELD OF ONCOLOGY. CONSIDERING THE WELL-ESTABLISHED SAFETY RECORD AND EFFICACY IN ANTI-MALARIAL TREATMENT, ALONG WITH ITS EMERGING ANTI-CANCER PROPERTIES, ARTESUNATE (ART) CAN FORM THE BASIS OF NOVEL TREATMENT REGIMEN FOR VARIOUS MALIGNANCIES. HENCE, THE ANTI-TUMOR EFFECT(S) OF ART IN PCA WERE SYSTEMATICALLY INVESTIGATED IN THE PRESENT STUDY. OUR IN-SILICO DATA REVEALED NF-?B AS A POTENTIAL TARGET OF ART IN PCA TUMOR CELL PLATFORM, AND STAT3, THE MAJOR DOWNSTREAM MOLECULE THAT WAS AFFECTED BY ART-MEDIATED INHIBITION OF THE NF-?B SIGNALING PATHWAY. ACCUMULATING EVIDENCE(S) FROM THE EXISTING LITERATURE CLEARLY SUGGEST AN ASSOCIATION BETWEEN ANDROGEN RESISTANCE AND THE EXISTENCE OF A FEED FORWARD LOOP WITH IL-6, NF-?B AND STAT3. CONSIDERING THE RESULTS FROM OUR IN-VITRO EXPERIMENTAL MODELS, IT IS COMPELLIN
dc.language.isoen
dc.subjectArtesunate, Prostate cancer, STAT3, Nuclear factor - kappa B, xenograft, TRAMP
dc.typeThesis
dc.contributor.departmentPHARMACOLOGY
dc.contributor.supervisorGautam Sethi
dc.contributor.supervisorGautam Sethi
dc.description.degreePh.D
dc.description.degreeconferredDOCTOR OF PHILOSOPHY (SOM)
dc.identifier.isiutNOT_IN_WOS
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