| Summary: | Advanced prostate cancer (PCa) treatment remains challenging, requiring new drug targets and therapies to improve outcomes for patients. Studies have linked ABCC5 overexpression to unfavourable tumour grading, shortened recurrence-free survival, and reduced overall survival in PCa. However, the precise mechanisms and pathways governed by ABCC5 in the context of PCa remain elusive. This thesis aims to advance our comprehension of ABCC5’s role in PCa as limitations persist due to the scarcity of in-depth functional studies and the absence of the ABCC5 crystal structure. This study proposes a novel dual perspective, suggesting that shorter ABCC5 isoforms might be responsible for epigenomic regulation, particularly within the nucleus, while protein from full-length transcripts could play a distinct role in mitochondria, associated with heme metabolism and apoptosis. The categorisation of ABCC5’s roles into these two compartments offers a fresh insight into its potential functionality, contributing to our understanding of its diverse impact on PCa biology. In the nucleus, ABCC5 impacts pathways related to SUMOylation and cell cycle regulation. Whereas, in the mitochondria, promoter analysis emphasises ABCC5’s connection to the heme metabolism, while caspases in the protein network highlight ABCC5’s participation in mitochondrial apoptotic pathways. Further, structural similarities with PCAT1 raise questions about an enzymatic function and potential protein modification mediated by ABCC5. Future research should explore these novel targets and investigate this proposed dual functionality to deepen our comprehension of ABCC5’s function in PCa.
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