ZNF200 interacts with DDX17 to regulate the transcriptional activity of RBP-J. [ChIP-Seq]

In order to explore the molecular mechanism of ZNF200 in the development of NSCLC, we conducted CUT&Tag experiments in the H1299 cell line using IgG and ZNF200 antibodies. Based on previous exploratory experiments, we found an interaction between DDX17 and ZNF200. Therefore, we stably transfected DDX17-HA into H1299 cells and performed CUT&Tag experiments using IgG and ZNF200 antibodies. We then discovered that both ZNF200 and DDX17 act on the promoter region of RBP-J. Consequently, in the DDX17-HA stable transfectants of H1299,H520 and A549 cells, we knocked down ZNF200 and performed CUT&Tag experiments using HA antibodies. At the same time, we knocked down ZNF200 and DDX17 in the H520and A549 cell lines, respectively. Since H3K4me3, as an epigenetic modification, is a hallmark of the active status of gene promoter regions and is usually associated with the activation of gene expression, we subsequently used antibodies against histone H3K4me3 for the CUT&Tag experiments. Overall design: CUT&Tag of IgG and ZNF200 in H1299 cells, CUT&Tag of IgG and ZNF200 after stable transfection of DDX17-HA in H1299 cells, and after knocking down ZNF200 in H1299,H520 and A549 cells stably transfected with DDX17-HA, as well as CUT&Tag of HA, and also knocking down ZNF200 and DDX17 in H520 and A549 cell lines compared to the control group for H3K4me3 CUT&Tag.