LncRNA CCAT1 promotes prostate cancer cell proliferation by interacting with DDX5 and miR-28-5p

Abstract: Accumulated evidence indicates that CCAT1 functions as an oncogene in the progression of a variety of tumors. However, little is known as to how CCAT1 impacts tumorigenesis in human prostate cancer. In this study, we found from TCGA and MSKCC database that CCAT1 is highly upregulated in castration-resistant prostate cancer (CRPC) compared to androgen dependent prostate cancer (ADPC). Higher level of CCAT1 leads to increased mortality in CRPC patients. In vitro and in vivo studies show that CCAT1 promotes PCa cell proliferation as well as the tumor growth of PCa xenografts. Mechanistically, in cytoplasm, CCAT1 sponges miR-28-5p to prevent the anti-cancer effect. In nuclear, CCAT1 acts as a scaffold for DDX5 (P68) and AR transcriptional complex to facilitate the expression of AR regulated genes, thus stimulating CRPC progression. Our findings suggest that CCAT1 is an oncogenic factor in the progression of CRPC with different regulatory mechanisms in the nucleus and cytoplasm of cells.