CUT&Tag profiling of hnRNPK binding in H1299 lung adenocarcinoma cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE313771 | GEO | 2026/01/31
REPOSITORIES: GEO
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Project description:CUT&Tag profiling of hnRNPK binding in H1299 lung adenocarcinoma cells
| PRJNA1381577 | ENA
Project description:Purpose: The goals of this study are to invsetigate the primary biological process of HNRNPK. Methods: Briefly, samples (H1299 cells transfected with control or HNRNPK shRNA) were used to extract total RNAs for quality control and RNA-seq loading samples. RNA-seq was performed as DGE on an Illumia HiSeq platform and 50 bp paired-end reads were generated (BGI Co. Ltd.). Results: Gene Ontology (GO) analysis revealed that cell proliferation and migration were identified as the biological functions of HNRNPK Conclusions: RNA-seq in H1299 cell lines revealed that HNRNPK mainly regulated cell proliferation and migration.
2022-03-09 | GSE197946 | GEO
Project description:Purpose: The goals of this study are to invsetigate the primary signaling pathway enriched in CAFs after stimulation of LUAD supernatants. Methods: Briefly, the supernatants (HNRNPK knockdown and control) of H1299 cells were incubated with CAFs for 24h. Then the CAFs were used to extract total RNAs for quality control and RNA-seq loading samples. RNA-seq was performed as DGE on an Illumia HiSeq platform and 50 bp paired-end reads were generated (BGI Co. Ltd.). Results: Gene Ontology (GO) analysis revealed that cell proliferation and migration were identified as the biological functions of HNRNPK Conclusions: In CAFs, we confirmed that the PI3K-AKT signaling pathway was significantly enriched after stimulation of H1299 supernatants.
2022-03-02 | GSE197540 | GEO
Project description:Ewing sarcoma is a highly aggressive tumor characterized by a translocation between members of the FET family of RNA binding proteins and one of several ETS transcription factors, with the most common translocation being EWS-FLI1. EWS-FLI1 leads to changes in gene expression through mechanisms that are not completely understood. We performed RNA sequencing analysis on primary pediatric human mesenchymal progenitor cells (pMPCs) expressing EWS-FLI1 in order to identify novel target genes. This analysis identified lnc277 as a previously uncharacterized long non-coding RNA upregulated by EWS-FLI1 in pMPCs. Inhibiting the expression of lnc277 diminished the ability of Ewing sarcoma cell lines to proliferate and form colonies in soft agar whereas inhibiting lnc277 had no effect on other cell types tested. By analyzing gene expression after shRNA knockdown, we found that both EWS-FLI1 and lnc277 repressed many more genes that they induced and that a significant fraction of EWS-FLI1 repressed targets were also repressed by lnc277. Analysis of primary human Ewing sarcoma RNA sequencing data further supports a role for lnc277 in mediating gene repression. We identified hnRNPK as an RNA binding protein that interacts directly with lnc277. We found a significant overlap in the genes repressed by hnRNPK and those repressed by both EWS-FLI1 and lnc277, suggesting that hnRNPK participates in lnc277 mediated gene repression. Thus, lnc277 is a previously uncharacterized long non-coding RNA downstream of EWS-FLI1 that facilitates the development of Ewing sarcoma via the repression of target genes. Our studies identify a novel mechanism of oncogenesis downstream of a chromosomal translocation and underscore the importance of lncRNA-mediated gene repression as a mechanism of EWS-FLI1 transcriptional regulation. A673 Ewing cells expressing an shRNA targeting hnRNPK or control were subjected to paired end RNA sequencing and compared to shGFP control.
2014-11-01 | E-GEOD-60890 | biostudies-arrayexpress
Project description:RNA binding of CBFB and hnRNPK
| PRJNA490343 | ENA
Project description:Here, we report the first genomic-scale comprehensive characterization of mouse transcripts bound to hnRNPK. hnRNPK binding at the isoform level was evaluated via RNA-sequencing of liver samples obtained from obese and wild-type mouse models. The comparison of hnRNPK co-immunoprecipitated fractions with total RNA fractions in a given mouse model enabled quantitative evaluation of the binding affinity of hnRNPK for thousands of isoforms.
2015-10-01 | GSE65887 | GEO
Project description: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.
2026-02-26 | GSE309203 | GEO
Project description:ZBTB11 binding genes in NCI-H1299
2023-12-21 | GSE206958 | GEO
Project description:The nucleolus is the membraneless organelle in the nucleus mainly responsible for ribosome biogenesis. It is also an excellent stress sensor and any changes on its architecture or composition leads to nucleolar stress deriving in cell cycle arrest and interruption of ribosomal activity. However, nucleolar stress sustained is also a contributing factor to pathologies like aging and cancer, highlighting the importance of its homeostasis in the cells. In this study, we identified and described the pivotal role of the RNA-binding protein Hnrnpk in the ribosome biogenesis and nucleolar dynamics. We developed an in vitro model of Hnrnpk overexpression with CRISPR-Cas9/SAM and an in vivo mouse model of Hnrnpk ubiquitous overexpression. We found that this overexpression disrupted translation and caused alterations in the nucleolar structure, resulting in nucleolar stress with alterations in the levels and localization of the nucleolar components fibrillarin and nucleolin, as well as impaired ribosome biogenesis. These aberrations trigger cell cycle arrest and cell senescence, and the phenotype could be rescued with haploinsufficiency of p53, suggesting that it is a consequence of a p53-dependant nucleolar stress mechanism. Finally, in our mouse model, Hnrnpk overexpression led to an aging phenotype with bone marrow failure and reduced lifespan, similar to a ribosomopathy-like phenotype. Together, our findings identify Hnrnpk as a novel master regulator of ribosome biogenesis and nucleolar homeostasis through p53, providing a new view of the orchestration of nucleolar integrity, ribosome function and cellular senescence.
2025-06-04 | PXD046699 | Pride
Project description:ZBTB11 binding genes in NCI-H1299
| PRJNA853049 | ENA