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Abstract
ST6Gal-I sialyltransferase adds α2,6-linked sialic acids to the terminal ends of glycan chains of glycoproteins and glycolipids. ST6Gal-I is reportedly upregulated in many cancers, including hepatocellular carcinoma, ovarian cancer and breast cancer. However, the expression and function of ST6Gal-I in prostate cancer (PCa) and the mechanism underlying this function remain largely unknown. In this study, we observed that ST6Gal-I expression was upregulated in human PCa tissues compared to non-malignant prostate tissues. High ST6Gal-I expression was positively correlated with Gleason scores, seminal vesicle involvement and poor survival in patients with PCa. ST6Gal-I knockdown in aggressive prostate cancer PC-3 and DU145 cells significantly inhibited the proliferation, growth, migration and invasion capabilities of these cells. ST6Gal-I knockdown decreased the levels of several PI3K/Akt/GSK-3β/ β-catenin pathway components, such as p-PI3K, (Ser473)p-Akt, (Ser9)p-GSK-3β and β-catenin. Furthermore, targeting this pathway with a PI3K inhibitor or Akt RNA interference decreased p-Akt, p-GSK-3β and β-catenin expression, resulting in decreased PC-3 and DU145 proliferation, migration and invasion. Taken together, these results indicate that ST6Gal-I plays a critical role in cell proliferation and invasion via the PI3K/Akt/GSK-3β/β-catenin signaling pathway during PCa progression and that it might be a promising target for PCa prognosis determination and therapy.
Highlights
prostate cancer (PCa) is a growing public health problem worldwide and is the most common malignant neoplasm diagnosed in men in the United States and Western Europe, as well as the leading cause of death among men [1]
Targeting this pathway with a PI3K inhibitor or Akt RNA interference decreased p-Akt, p-Glycogen synthase kinase-3β (GSK-3β) and β-catenin expression, resulting in decreased PC-3 and DU145 proliferation, migration and invasion. These results indicate that ST6Gal-I plays a critical role in cell proliferation and invasion via the PI3K/Akt/GSK-3β/β-catenin signaling pathway during PCa progression and that it might be a promising target for PCa prognosis determination and therapy
These results suggest that ST6Gal-I overexpression is significantly associated with PCa progression
Summary
PCa is a growing public health problem worldwide and is the most common malignant neoplasm diagnosed in men in the United States and Western Europe, as well as the leading cause of death among men [1]. PCa is responsive to androgen ablation therapy and characterized by slow growth and usually remains confined to the prostate gland itself and causes only limited symptoms. As PCa advances, it often becomes androgen-refractory and spreads beyond the prostate and invades surrounding tissues. A metastatic PCa phenotype develops in affected patients [3]. Elucidating the molecular mechanism underlying PCa development and progression may be helpful in detecting the disease, as well as in determining patient prognosis and individualizing therapy
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