Abstract
Prostate cancer (Pca) is the second frequent malignancy in men. Long noncoding RNAs (lncRNAs) have been reported to play essential roles in the progression of cancers, including Pca. LncRNA colorectal neoplasia differentially expressed (CRNDE) has been found to affect tumorigenesis in many cancers. However, the exact role and mechanism of CRNDE in Pca remain poorly understood. 64 Pca patients were recruited in this study. PC3 and 22RV1 cells were used in vitro experiments. The expressions of CRNDE, microRNA-101 (miR-101), and Ras-related protein 1A (Rap1A) were detected in vivo and in vitro by quantitative real-time polymerase chain reaction and western blot, respectively. Cell proliferation, apoptosis, migration, and invasion were investigated through cell counting kit-8, flow cytometry, and Transwell assays, respectively. The interaction between miR-101 and CRNDE or Rap1A was explored by bioinformatics analysis and luciferase reporter assay. High expression of CRNDE was shown in Pca tissues and cells and predicted poor outcomes of patients. Overexpression of CRNDE promoted cell proliferation, migration, and invasion but decreased apoptosis in Pca cells, while its knockdown showed an opposite effect. CRNDE was a decoy of miR-101 and its effect on Pca progression was reversed by miR-101. Rap1A was identified as a target of miR-101 and it attenuated the effect of miR-101 on Pca development. Moreover, the Rap1A protein level was positively regulated by CRNDE, which was weakened by miR-101. CRNDE contributed to cell proliferation, migration, and invasion by regulating the miR-101/Rap1A axis in Pca, providing a novel strategy for Pca treatment.