Abirateron ve Docetaxel Tedavileri Metastatik Prostat Kanseri Hücrelerinde Phospho-PTEN Ekspresyonunu Arttırır

Abstract

Aim: Prostate cancer is the second leading cause of death in cancer-related deaths in men. Docetaxel and abiraterone acetate are widely used in the treatment of castration-resistant metastatic prostate cancer. Phospho-PTEN triggers proliferation, migration, angiogenesis and survival in cells by causing oncogenic Akt hyperactivation. This study, it is aimed to investigate the effects of docetaxel and abiraterone acetate agents, which are widely used in the treatment of prostate cancer, on the expression of phospho-PTEN, which stimulates the oncogenic pathway. Material and Methods: The effects of docetaxel and abiraterone acetate on phospho-PTEN expression in androgen receptor (+) and androgen receptor (-) metastatic prostate cancer cell lines were investigated in vitro by immunofluorescence method. Results: Findings were compatible in both androgen receptor (+) and androgen receptor (-) metastatic prostate cancer cell lines. No statistically significant difference in phospho-PTEN expression was observed between the control and abiraterone acetate groups. Phospho-PTEN expression was increased statistically significant in docetaxel and abiraterone acetate+docetaxel groups compared to control. This increase was greater statistically significant in the combined group given the two agents compared to the docetaxel group. Conclusion: A significant increase in phospho-PTEN was observed in the docetaxel and combined treatment groups. The increase of Phospho-PTEN causes oncogenic Akt hyperactivation. According to this information, docetaxel and combined drug treatments may support the oncogenic pathway in cells by increasing phospho-PTEN in patients. To eliminate these effects in patients, the administration of agents that dephosphorylate PTEN or agents that will stimulate the pathways that provide dephosphorylation may increase the total survival of the patients.