Prostate cancer ranks as the second most common cancer in men globally and represents a significant cause of cancer-related mortality. Metastasis, the spread of cancer cells from the primary site to distant organs, remains a major challenge in managing prostate cancer progression. Pyruvate dehydrogenase kinase 4 (PDK4) is implicated in regulating aerobic glycolysis and has emerged as a potential player in various cancer types, yet its role in prostate cancer remains poorly understood.

PDK4 expressions were detected by western blotting analysis and real time PCR from cell lines and human tissues samples. Migration ability was analyzed by matrigel coated invasion chambers. Human sampled were collected from Chilgok Kyungpook National University Hospital.

We found elevated expression of PDK4 in prostate cancer cell lines compared to normal prostate cells, with particularly high levels observed in DU145 and LnCap cell lines. Knockdown of PDK4 in these cell lines resulted in suppressed invasion ability, indicating a potential role for PDK4 in prostate cancer metastasis. Furthermore, our results revealed alterations in epithelial-mesenchymal transition (EMT) markers and downstream signaling molecules following PDK4 suppression, suggesting its involvement in modulating invasion-related pathways. Analysis of patient tissue samples confirmed elevated PDK4 expression in prostate cancer tissues compared to normal prostate tissues, and PSA and PDK4 expression showed significantly positive correlation.

Overall, our findings suggest that PDK4 may contribute to prostate cancer tumorigenesis and progression, highlighting its potential as a therapeutic target for combating this disease.