![]() Therefore, it is critical to address the limitations of clinical treatments for patients with advanced PCa by exploring the underlying molecular mechanism of PCa progression. CRPC is characterized by a poor prognosis and limited therapeutic efficacy. However, with the continuous progression of the disease, most PCa patients who have received ADT will inevitably show progression to castration-resistant prostate cancer (CRPC) after 18–24 months. Androgen deprivation therapy (ADT) is the cornerstone of PCa treatments and is also the dominant therapy for advanced PCa. Under these conditions, radical resection cannot be performed. In China, approximately half of PCa patients are diagnosed at the late stage. Radical prostatectomy (laparoscopic or robot-assisted approaches) and radiotherapy have remained the gold standard for localized PCa treatment. Prostate cancer (PCa) is one of the most common malignancies in men. ADPGK accelerates PCa glycolysis and progression by activating ALDOC-AMPK signaling, suggesting that ADPGK might be an effective target and marker for PCa treatment and prognosis evaluation. In summary, ADPGK is a driving factor in PCa progression, and its high expression contributes to a poor prognosis in PCa patients. ALDOC was positively correlated with ADPGK, and high ALDOC expression was associated with worse survival outcomes in PCa. ![]() Mechanistically, ADPGK binds aldolase C (ALDOC) to promote glycolysis via AMP-activated protein kinase (AMPK) phosphorylation. Metabolomics, proteomics, and ECAR and OCR tests revealed that ADPGK significantly accelerated glycolysis in PCa. In vitro and in vivo experiments showed that ADPGK overexpression promoted PCa cell proliferation and migration, and ADPGK inhibition suppressed malignant phenotypes. High ADPGK expression indicates worse survival outcomes, and ADPGK serves as an independent factor of biochemical recurrence. Clinical sample analysis demonstrated that ADPGK was markedly upregulated in PCa tissues vs. ResultsĪDPGK was the only glucokinase that was both upregulated and predicted worse overall survival (OS) in prostate adenocarcinoma (PRAD). The underlying mechanisms were explored through ADPGK overexpression and knockdown, co-immunoprecipitation (Co-IP), ECAR analysis and cell counting kit-8 (CCK-8) assays. Quantitative proteomics, metabolomics, and extracellular acidification rate (ECAR) and oxygen consumption rate (OCR) tests were performed to evaluate the impact of ADPGK on PCa metabolism. ![]() The effect of ADPGK expression on PCa cell malignant phenotypes was validated in vitro and in vivo. The Cancer Genome Atlas (TCGA) database, online tools and clinical samples were used to assess the expression and prognostic role of ADP-dependent glucokinase (ADPGK) in PCa. We aimed to investigate the role of hexokinases in prostate cancer (PCa) and identify a crucial target for PCa treatment. Cell metabolism plays a pivotal role in tumor progression, and targeting cancer metabolism might effectively kill cancer cells.
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