Search

Circular RNAs (circRNAs) participate in the progression of various cancers. However, the function of circ_0062019 in prostate cancer (PCa) remains unclear. In this study, CCK‐8, colony formation, transwell, tube formation and flow cytometry assays were applied to assess cell proliferation, motility, angiogenesis, cell cycle distribution and apoptosis. The binding association between miR‐1253 and circ_0062019 or NRBP1 was verified through dual‐luciferase reporter assay and RIP assay. Xenograft assay was conducted to evaluate tumour formation in vivo. As a result, circ_0062019 and NRBP1 were increased, but miR‐1253 was decreased in PCa. Depletion of circ_0062019 curbed cell proliferation, migration, invasion, angiogenesis and EMT and induced apoptosis in PCa cells. Circ_0062019 facilitated the malignancy of PCa cells via sequestering miR‐1253. Simultaneously, miR‐1253 hindered PCa cell progression via regulating NRBP1. Ccirc_0062019 silencing suppressed tumour growth in vivo. Taken together, circ_0062019 expedited PCa progression through mediating miR‐1253/NRBP1 pathway. [ABSTRACT FROM AUTHOR]

PRDM14 (PRDI-BF1 and RIZ domain-containing 14), a transcription factor, plays important roles in primordial germ cell specification and embryonic stem cell pluripotency, and supports the maintenance of self-renewal by promoting the expression of stem cell markers while also repressing the expression of differentiation factors. As a proto-oncogene, the ectopic expression of PRDM14 can enhance breast cell growth and reduce breast cell sensitivity to chemotherapeutic drugs. Conversely, knockdown of PRDM14 expression induces apoptosis in breast cancer cells and restores their sensitivity to chemotherapeutic drugs. Here, we sought to identify the role of PRDM14 in 293T cells. PRDM14-infected 293T cells exhibited an abnormal morphology, and we found that ectopic expression of PRDM14 inhibits colony formation, cell proliferation and metastasis. In addition, our data indicated that PRDM14 influences the G1/S phase transition of 293T cells by inducing the expression of cell cycle regulators. In conclusion, these results showed that PRDM14 inhibits 293T cell proliferation by influencing the G1/S phase transition and impacts cell migration by regulating the level of MMP/TIMP expression, thus mediating extracellular matrix degradation. [ABSTRACT FROM AUTHOR]

PRDM1 (PR domain containing 1) is a transcriptional repressor that affects the expression of numerous genes involved in cell proliferation, differentiation and metabolism. However, the molecular mechanisms underlying PRDM1-regulated gene expression in the DF-1 cell line remain to be elucidated. In this study, we explored the role of PRDM1 in cell proliferation and cell cycle by forced expression of PRDM1 in DF-1 cells. Our results showed an absence of endogenous PRDM1 in this cell line, while exogenous PRDM1 was specifically localized to the nucleus. Ectopic expression of PRDM1 inhibited DF-1 cell proliferation and altered clonal morphology. Furthermore, PRDM1 overexpression caused an increase in the G0/G1 phase population. The levels of p53 mRNA and the p53-regulated p21 WAF1 and MDM2 genes were significantly increased in DF-1 cells transfected with the PRDM1 expression vector. Examination of the Rb pathway further revealed that Rb, E2F-1 and p15 INK4b alternate reading frame (ARF) mRNA were also significantly increased after transient transfection. Interestingly, the mRNA expression levels of multiple chicken cyclin genes were also increased. These results show that PRDM1 overexpression induced G0/G1 arrest in DF-1 cells through multiple parallel mechanisms, including the p53 and Rb pathways. [ABSTRACT FROM AUTHOR]