Document Type : Short Communication
Institute of Health Sciences, Istanbul University, Istanbul, Turkey
Department of Basic Oncology, Istanbul University Oncology Institute, Istanbul, Turkey
Department of Immunology, Istanbul University Aziz Sancar Institute of Experimental 7 Medicine, Istanbul, Turkey
Prostate cancer (PCa) is a common malignant disease with high mortality rates that develops and progresses in an
androgen-dependent way. In recent years, RNA sequencing enabled identification of many PCa-related long noncoding
RNAs including androgen receptor-regulated long non-coding RNA 1 (ARLNC1) and prostate cancer-associated
transcript 1 (PCAT1). In the present study, our goal was to illuminate expression changes of ARLNC1 and PCAT1 in
the context of androgen stimulation or androgen receptor (AR) blockade with respect to AR expression status. In this
experimental study, LNCaP cells and higher AR-expressing LNCaP-AR++ cells were used as cell models. Cells were
treated with dihydrotestosterone (DHT) as an androgen stimulator and/or enzalutamide as an AR inhibitor. Cell viability
was assessed using annexin V and propidium iodide (PI) staining in flow cytometry. Androgen stimulation prompted
baseline ARLNC1 levels by 53.5-fold in the LNCaP cells (P=0.01) and by 25-fold in the LNCAP-AR+ cells (P=0.18). AR
inhibition by enzalutamide reduced baseline ARLNC1 in LNCaP-AR++ cells by 2-fold (P=0.01), but to a lesser extent
in LNCaP cells. Co-treatment of cells with DHT and enzalutamide led to a remarkable decrease in the DHT effect on
ARLNC1 expression. No specific effect of androgen stimulation or AR blockade on PCAT1 expression was detected.
Our results revealed that the extent of induction of ARLNC1 by androgen is modulated by receptor expression status.
In addition, we determined that AR blockade, via enzalutamide, effectively suppresses ARLNC1 both at baseline and
after induction by DHT.