Project description:To explore whether DANCR plays a role in nasopharyngeal carcinoma tumorigenesis, a RNA-seq analysis was performed to compare the gene expression profiles of DANCR siRNA and control groups.
Project description:The prognosis for bladder cancer (BCa) patients with lymph node (LN) metastasis is forlorn and restrainedly improved by current treatment. DANCR is reported to play a role in prostate cancer and liver cancer. However, its function and underlying mechanism in BCa remains unknown. The goal of this study is to identify the target genes of DANCR in bladder cancer. Our results indicate that the genes regulated by DANCR are involved in a variety of biological functions, such as proliferation and metastasis.
Project description:BackgroundLong noncoding RNAs (lncRNAs) are a new class of cancer regulators. Here, we aimed to investigate the diagnostic and therapeutic values of an lncRNA, differentiation antagonizing noncoding RNA (DANCR), in lung cancer.MethodsReal-time polymerase chain reaction was used to compare DANCR levels in normal and cancerous lung tissues as well as lung cancer cells. Lentiviral transduction was used to induce DANCR overexpression or silencing in vitro, followed by monitoring cell proliferation, colony formation, and changes in microRNA-216a (miR-216a) expression. DANCR-specific small hairpin RNA transduction was used to establish cells with stable DANCR knockdown, and silenced cells were used to initiate lung tumor xenografts, followed by monitoring tumor growth.ResultsDANCR upregulation was seen in lung cancer, particularly in high-grade lung cancer tissues and aggressive cancer cells. Ectopic DANCR expression induced lung cancer cell proliferation and colony formation, whereas DANCR silencing induced opposing effects. The miR-216a level in cancer cells was negatively correlated with DANCR expression. The DANCR knockdown reduced the growth of tumor xenografts in vivo.ConclusionDANCR upregulation is a potential indicator of aggressive lung cancer. Silencing of DANCR has great potential as a potent therapeutic strategy in lung cancer.
Project description:Cancer cell autophagy has been associated with the progression of gastric cancer (GC), but involvement of long noncoding RNAs (lncRNAs) remains unclear. Initial bioinformatics analysis has identified abnormally highly expressed KLF5 in GC, as well as the predicted regulatory mechanism associating with lncRNA DANCR, miR-194, and AKT2. The expression of KLF5, DANCR, and AKT2 in GC tissue was upregulated, and the expression of miR-194 was downregulated. We knocked KLF5 down and manipulated the expression of DANCR, miR-194, and AKT2 to characterize their roles in GC cell viability, autophagy, and apoptosis. The mechanistic investigations revealed that KLF5 activated the transcription of DANCR in the promoter region and elevated its expression. DANCR acted as a miR-194 sponge to repress its expression in GC. MiR-194 targeted and inhibited AKT2 expression. Silencing KLF5 augmented GC cell autophagy, apoptosis and impeded its viability through the DANCR/miR-194/AKT2 axis. The tumor-inhibiting properties of KLF5 knockdown were substantiated in vivo. Together, our study uncovered the oncogenic role of KLF5-dependent lncRNA DANCR transcription in GC in vivo and in vitro, which implicates the miR-194/AKT2 axis in tumor growth regulation, and it may be a potential therapeutic target for human GC.
Project description:To investigate the cooperative function NCoR/HDAC3/PGC1β complex in the regulation of osteoclast differentiation, we used NCoR KO or PGC1β KO bone marrow cells and non-coding RNA Dancr/Rnu12 siRNA knockdown bone marrow cells or RAW 264.7 cells. We selected Dancr and Rnu12 as non-coding RNAs to knockdown based on results from an eCLIP essay.
Project description:Increasing evidence indicates that long noncoding RNAs (lncRNAs) function as important regulators in biological processes and are dysregulated in various tumors. The lncRNA DANCR functions as an oncogene in various cancers, but elucidation of its role in pancreatic cancer (PC) requires further investigation. In the current study, we demonstrate that DANCR was increased in PC tissues and cell lines. Knockdown of DANCR significantly suppressed cell proliferation, migration, and invasion and influenced the levels of epithelial-to-mesenchymal transition-associated proteins, as demonstrated by the observation of enhanced E-cadherin levels and reduced N-cadherin levels in PC cells. In addition, we identified direct binding to the predicted miR-33b binding site on DANCR. We also showed that there is reciprocal repression between DANCR and miR-33b. Furthermore, a miR-33b inhibitor partially abrogated knockdown of DANCR and caused inhibitory effects. We also demonstrated that DANCR functions as a miR-33b sponge to positively regulate MMP16 expression in PC cells. Collectively, the data reveal that DANCR exerts its function by regulating miR-33b/MMP16 expression, implying an important role for a lncRNA-miRNA-mRNA functional network and suggesting a novel potential therapeutic target for PC.