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.

To investigate the mechanism of antiprogestins in the regulation of ovarian function, a dual-chamber culture system was prepared with the amnion membrane of human placenta. Isolated porcine granulosa and thecal cells were grown on both sides of the amnion and co-cultured with or without RU486 and ZK98, 734. After 48 h incubation, the progesterone receptor (PR) and estrogen receptor (ER) of both cells were detected by flow cytometry. Progesterone and estradiol concentrations in the media were measured by radioimmunoassay. The results showed that antiprogestins increased PR contents in both cells; no significant change was found for ER. At the same time the progesterone and estradiol production by granulosa cells was inhibited; the progesterone production by thecal cells was reduced also. These data suggest that progesterone regulates progesterone synthesis. This autocrine/paracrine action may be the approach through which progesterone controls PR upregulation. It could be one mechanism for the inhibition of follicle development and steroidogenic function by antiprogestins.