ARTESUNATE SUPPRESSES TUMOR GROWTH AND PROGRESSION OF PROSTRATE CANCER THROUGH THE MODULATION OF STAT3 AND NF-kB SIGNALING CASCADES

Abstract

DRUG 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