Project description:We profile gene expression upon circCDYL KD in HepG2 cells and in two bladder cancer cell lines J82 and UMUC3 as well as upon knockdown of the RNA binding proteins (RBP) GRWD1, IGF2BP1, and IGF2BP2 in J82 and UMUC3
Project description:RNA-Seq of circCDYL knockdown (KD) samples in HepG2, J82, and UMUC3 cells and of GRWD1, IGF2BP1, and IGF2BP2 knockdown (KD) samples in J82 and UMUC3 cells
Project description:To uncover the dysregulated genes in BCa, we performed the RNA-seq to detect the gene expression levels in four BCa cells (5637, UMUC3, T24, and J82) and human immortalized urothelial cell SV-HUC-1. To search for the differentially expressed genes of for cell lines (5637, J82, UMUC3, and T24) compared to the normal cell line SV-HUC-1.
Project description:To investigate gene expression profile changes after ANLN knockdown, we have employed whole genome microarray expression profiling as a discovery platform to identify genes that altered after ANLN knockdown, so as to explore the potential function of ANLN. Bladder cancer cell line J82 was knocked down by using small interfering RNA (siRNA) or control siRNA 24, 48 and 72 hours, respectively.
Project description:circHIPK3 silencing impairs ß-cell functions leading to a decrease in insulin secretion, proliferation, and survival. Therefore, we wanted to identify the mode of action of circHIPK3 by measuring gene expression changes upon circHIPK3 silencing in MIN6B1 cells.
Project description:Aortic valve calcific disease (CAVD) is a common heart valve condition typically characterized by severe narrowing of the aortic valve. Our previous research has shown that circHIPK3 is downregulated in calcified aortic valve tissues and plays a role in regulating the progression of CAVD. To further investigate how circHIPK3 exerts its inhibitory effects on aortic valve calcification, we overexpressed circHIPK3 in aortic valve interstitial cells and conducted RNA-seq analysis, revealing that circHIPK3 regulates key factors in the Wnt signaling pathway. These findings contribute to a deeper understanding of the molecular mechanisms underlying CAVD, particularly the potential involvement of circRNAs in this disease.