Abstract

Drug resistance is the leading cause of death in prostate cancer patients. Therefore, exploring the mechanism underlying drug resistance of prostate cancer and identifying novel therapeutic targets are urgently needed. Long non-coding ribonucleic acid disrupted in renal carcinoma 3 acts as a tumor suppressor gene in several tumor types. However, to date, no study has investigated the biological function of long non-coding ribonucleic acid disrupted in renal carcinoma 3 in prostate cancer. Gene expression was detected by reverse transcription-quantitative polymerase chain reaction assay and Western blot. Cell viability was detected by cell counting kit-8 assay and cell apoptosis was analyzed by flow cytometry. The interactions between long non-coding ribonucleic acid and microRNA, microRNA and messengerRNA were analyzed by bioinformatics analysis and confirmed by a dual-luciferase reporter gene assay. Long non-coding ribonucleic acid disrupted in renal carcinoma 3 was down-regulated in drug-resistant prostate cancer tissues and cell lines. Over expression of long non-coding ribonucleic acid disrupted in renal carcinoma 3 overcome the drug resistance of PC-3/R and DU-145/R to docetaxel by down-regulating drugresistance related lung resistance protein, P-glycoprotein and multidrug resistance-associated protein. Long non-coding ribonucleic acid disrupted in renal carcinoma 3 sponged microRNA-24-3p in PC-3/R and DU-145/R to up-regulate KIT ligand. MicroRNA-24-3p/KIT ligand mediated the effect of long noncoding ribonucleic acid disrupted in renal carcinoma 3 overexpression on docetaxel-resistance of prostate cancer cells. Long non-coding ribonucleic acid disrupted in renal carcinoma 3 overcome drug resistance of docetaxel-tolerated prostate cancer cells to docetaxel via the microRNA-24-3p/KIT ligand axis. Our study revealed that long non-coding ribonucleic acid disrupted in renal carcinoma 3 was a potential therapeutic target in overcoming docetaxel resistance for prostate cancer patients.