Androgen deprivation‑induced OPHN1 amplification promotes castration‑resistant prostate cancer.

Androgen deprivation therapy (ADT) is used to treat prostate cancer (PCa). However, ADT may increase the expression of androgen receptor () through the amplification of chromosome X. The gene oligophrenin 1 () is located in the same region as the gene, which could be amplified by ADT. Thus, the role of in PCa pathology was investigated. The expression status of in PCa was searched in The Cancer Genome Atlas (TCGA) database. Androgen‑sensitive cells LNCaP and 22RV1 were cultured under ADT conditions, and then the expression of was evaluated by northern blotting. The expression of was enhanced or knocked down in LNCaP and 22RV1 cells by transfection. Subsequently, the LNCaP and 22RV1 cells were cultured under ADT, and the viability rate, apoptosis, and migration of cells were assessed by MTT, flow cytometry, and Transwell assay respectively. The expression of was also enhanced or knocked down in androgen‑insensitive PC3 cells, and then the effects of OPHN1 on the viability, apoptosis, and migration of PC3 cells were assessed. A mouse xenograft model was created by injecting LNCaP cells with overexpression subcutaneously, and the tumor growth rates were monitored. In TCGA database, amplification of the gene was observed in the PCa tumors. ADT increased the expression of in LNCaP and 22RV1 cells (P<0.05). could promote resistance of LNCaP and 22RV1 cells to ADT by promoting cell survival and preventing their apoptosis (P<0.05). In addition, contributed to cell viability (P<0.05) and enhanced the migration ability in LNCaP, 22RV1 and PC3 cells (P<0.05). In the mouse model, the PCa xenograft with overexpression had a higher growth rate and was more resistant to the ADT condition (P<0.05). In summary, ADT induced the overexpression of in PCa, which facilitated PCa cell survival and promoted PCa progression.