Prostate cancer is one of the most common
malignancies in men and is predicted to be the second leading cause of
cancer-related deaths. After 6-18 months,
hormone ablation treatment results in
androgen-independent growth of
cancer cells,
metastasis and progression. The mechanism of
androgen-independent growth of prostatic
carcinoma cells is still unknown. Identification of factors that facilitate the transition from
androgen-dependent to independent states is crucial in designing future diagnostics and medication strategies. To understand the biochemical meaning of
hormone dependency deprivation,
glycoproteins enriched profiles were compared between DU145 (
hormone non-responding) and LNCaP (
hormone responding)
prostate cancer cells. These results allow for anticipation on the important role of glycosylation in malignant transformation. Both
Tn antigen and complex antennary N-
oligosaccharides were recognized. Their occurrence might be involved in the development and progression of
tumor, and failure of
hormone ablation
therapy. Among identified
proteins in
androgen-sensitive cells
nucleolin (P19338) was found that is widely described as apoptosis inhibitor, and also transporter of molecules from the membrane to the cytoplasm or nucleus. In addition,
14-3-3 protein family (P27348, P31946, P61981, P63104, P62258, Q04917, and P31947) was investigated across available databases as it forms stable complexes with
glycoproteins. Our studies indicate that
isoforms: sigma and eta were found in
androgen-dependent
prostate cancer cells, while other
isoforms were present in
androgen non-responding cells. 14-3-3 binding partners are involved in
cancer pathogenesis. These findings may contribute to a better understanding of
prostate cancer tumorigenesis and to a more efficient prognosis and individual
therapy in a future. However, it still remains to be revealed how important those changes are for
androgen dependency loss in
prostate cancer patients carried out on clinically relevant populations.