CA916798 affects growth and metastasis of androgen-dependent prostate cancer cells

OBJECTIVE: Abnormal activation of androgen receptor (AR) signaling pathway is a critical pathogenic mechanism and therapeutic target for prostate cancer (PCa). The CA916798 is a tumor-associated gene and may be regulated by the androgen-AR pathway. This study aims to investigate the function of CA916798 in the growth and metastasis of androgen-dependent PCa cells.

MATERIALS AND METHODS: CA916798 expression in PCa cell lines was investigated. LNCap cells were divided into 4 groups: LNCap, LNCap+ Dihydrotestosterone (DHT), LNCap+DHT+siCA916798, and LNCap+DHT+siRA group. CA916798 expressions in LNCap cells treated with siCA917698 or siAR were examined. The viability, apoptosis, migration, and invasion of PCa cells were examined. Dual luciferase and ChIP assays were used to examine the interaction between the AR and CA916798.

RESULTS: Endogenous CA916798 mRNA levels in PC3 cells were significantly higher than those in LNCap cells (p < 0.05). However, CA916798 was androgen-sensitive in LNCap cells, but not in PC-3 cells. Dual luciferase and ChIP assays showed that AR could specifically bind to the promoter regions of the CA916798. Knockdown of CA916798 (LNCap+DHT+siCA916798) and AR (LNCap+DHT+siAR) resulted in decreased cell viability, migration, and invasion, while it induced apoptosis and G1 cell cycle arrest in LNCap cells.

CONCLUSIONS: DHT could initiate the transcription of CA916798, which further mediates the androgen-AR signaling pathway-dependent cell growth and metastasis of the prostate cancer cell line LNCap.

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