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Prostate cancer is the second leading cause of cancer deaths in the USA. Current treatment strategies include Androgen deprivation therapy (ADT) followed by radio and chemotherapy which later resulted in drug resistance. The key to managing prostate cancer is to understand what drives progression and how to stop it. Arginyltransferase 1 (Ate1), an enzyme mediating post-translational protein arginylation, which has recently been identified as a master regulator affecting many cancer-relevant pathways including stress response, cell cycle checkpoints, and cell migration/adhesion. Earlier study in our lab, we have discovered that downregulation of ATE1 is an important factor in PC progression and metastasis. However, the precise role of ATE1 in drug resistance condition is unknown and therefore the present study focused to investigate the role of ATE1 in drug resistance in different prostate cancer cells. For this study, we have used non-metastatic and metastatic cell lines such as LnCAP, DU145 and PC3 and checked the expression and level of ATE1 and the cell viability assay followed by treatment with second line chemotherapeutic agents such as docetaxel or paclitaxel. In addition, we have also made stable knockdown of ATE1 in those cell lines and tested by treating with chemotherapeutic agents docetaxel or paclitaxel and measured the cell viability. Our findings showed that metastatic cells which possessed very low levels of ATE1 showed more resistance towards chemotherapeutic treatment. Further, we have also analyzed through ATE1shRNA cells showed more resistance towards taxols treatment when compared to the Scrambled ShRNA cells. Overall, our findings showed that the presence of ATE1 is more important for the sensitivity of chemotherapeutic agents to stop the metastasis.
Sriramajayam et al. (Fri,) studied this question.