Impact of BCL2 Overexpression in castration resistance prostate cancer progression I
In analyzing transcriptomic data from a clinical trial of neoadjuvant-intensive Androgen Deprivation Therapy, we observed increased mRNA expression of the hallmark antiapoptotic gene BCL2 in the prostate tumors of treated patients versus those of untreated patients.  We showed that BCL2 overexpressed LNCaP cells exhibited resistance to prolonged androgen deprivation therapy, indicating that BCL2-overexpression leads to castration resistance and cellular plasticity.Our study indicating that BCL2 overexpression may act as a major driver of early castration resistance in prostate cancer cells. Overall design: To investigate the function of BCL2, we stably overexpressed humna BCL2 in prostate cancer cells. We grow the isogenic pairs of cells to androgen deprivation for a prolonged time (28 days) and perfermed RNA sequencing