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Transcriptomic analysis of ZHX3-depleted HepG2 cells

ABSTRACT: The aim of this RNA-Seq analysis was to identify target genes of the transcription repressor ZHX3 in HepG2 cells. To do so, four stable lines were generated in HepG2 using three different ZHX3-targeting CRISPR constructs and an empty vector construct. Bulk RNA-Seq analysis was performed on these four lines. Sequencing was done by NovogeneAIT Genomics using the Illumina® NovaSeq6000-PE150 platform and 63-82 million base pairs were sequenced per sample. A total of 47 and 156 genes were found to be consistently upregulated and downregulated (fold change ≥ 2 and FDR < 0.05), respectively, in all three KO lines as compared to the empty control line. Functional enrichment analysis of the 156 upregulated genes using g:profiler revealed the enrichment of two biological processess, urate transport and urate metabolic process. qPCR analysis validated the upregulation of uric acid transporter gene SLC17A1.

ORGANISM(S): Homo sapiens

PROVIDER: GSE193872 | GEO | 2025/02/26

REPOSITORIES: GEO

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ZHX3 interacts with CEBPB to repress hepatic gluconeogenic gene expression and uric acid secretion

Project description:ZHX3, which encodes for a transcriptional repressor, is associated with fasting blood glucose (FBG) levels and increased type 2 diabetes (T2D) risk but its role in cell types involved in glucose metabolism is not well understood. Here, we show that the deletion of ZHX3 in the human pancreatic β cell line EndoC-βH1 did not impair glucose-stimulated insulin secretion (GSIS) nor perturb its transcriptome. On the other hand, we found that ZHX3 represses the expression of gluconeogenic genes PCK1 and G6PC1 in the human hepatoma line HepG2. Transcriptomic analysis of ZHX3-deficient HepG2 cells revealed that the uric acid transporter gene SLC17A1 was upregulated, which consequentially led to increased uric acid secretion. High levels of uric acid could then impair GSIS in EndoC-βH1 cells. Subsequently, in-depth co-immunoprecipitation followed by mass spectrometry analysis of ZHX3 in HepG2 cells identified transcription factor CEBPB as its binding partner, required to repress the transcription of PCK1, G6PC1 and partially SLC17A1 in HepG2 cells. Overall, our study uncovered the role of ZHX3 in regulating glucose metabolism in hepatocytes, thereby influencing FBG levels and its association with T2D risk.

2026-04-27 | PXD046714 | Pride

Transcriptomic analysis of ZHX3-depleted HepG2 cells

Project description:Transcriptomic analysis of ZHX3-depleted HepG2 cells

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Genome-wide distribution of ZHX3 in human fibroblast cells.

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Effect of deletion of ZHX3 on gene expression in human pancreatic beta cells EndoC-BH1

Project description:ZHX3 is a transcriptional factor whose role in human pancreatic beta cells is not well understood. In attempt to identify the genes that ZHX3 regulates in beta cells, we KO ZHX3 using CRISPR in EndoC-βH1 cells and performed RNA-Seq. We have only identified 36 and 31 genes that were significantly up and downregulated respectively. This is in concordance with our functional data whereby the KO of ZHX3 in EndoC-βH1 did not affect its insulin secretory function. Overall, we conclude that the KO of ZHX3 did not result in major perturbations in EndoC-βH1 cells.

2025-02-26 | GSE236102 | GEO

lncRNA-operated stem cell fate control: RPS3 organizes the in situ Gm16751-Zhx3 interactome to program spermatogonial differentiation [RIC-Seq]

Project description:Long non-coding RNAs (lncRNAs) play pivotal regulatory roles in mammalian male gametogenesis. Advances in high-throughput technologies have demonstrated that lncRNAs orchestrate robust, flexible, and context-specific gene regulatory networks through dynamic interactions with proteins, DNA, and RNA, modulating transcriptional and post-transcriptional processes. However, the mechanistic role of in situ lncRNA-mRNA interactions in spermatogonial stem cell (SSC) differentiation remains poorly understood. In this study, we employed RIC-seq (RNA in situ conformation sequencing) and LongRNA-seq to systematically identify a functional interaction between lncRNA Gm16751 and Zhx3 mRNA during SSC differentiation, which was further visualized via a Circos plot. Mechanistically, we demonstrated that Gm16751 enhances the mRNA stability of Zhx3, thereby promoting SSC differentiation. Furthermore, mass spectrometry analysis revealed that RPS3 (Ribosomal Protein S3) serves as a critical RNA-binding protein (RBP) that bridges the interaction between Gm16751 and Zhx3, ultimately stabilizing Zhx3 mRNA and modulating SSC differentiation. Our findings provide novel mechanistic insights into the lncRNA-mRNA regulatory axis in SSC differentiation and establish a foundation for understanding the molecular etiology of male germ cell developmental disorders and spermatogenic dysfunction.

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lncRNA-operated stem cell fate control: RPS3 organizes the in situ Gm16751-Zhx3 interactome to program spermatogonial differentiation [Long RNA-Seq]

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Genome-wide distribution of ZHX3 in human fibroblast cells.

Project description:Genome-wide distribution of ZHX3 in human fibroblast cells.

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Allantoin promotes MASLD progression

Project description:Uric acid has garnered increasing attention for its association with metabolic dysfunction-associated steatotic liver disease (MASLD) in recent cross-sectional studies, although detailed understanding of its involvement remains limited. This study confirms a strong association between urate levels and elevated risk of both MASLD and type 2 diabetes (T2D) through a large-scale observational analysis of UK Biobank data. However, Mendelian randomization (MR) analysis involving over 2 million samples identified only causal effects of urate on serum triglyceride levels and the risk of T2D. Additionally, a targeted metabolomics study involving elderly Chinese participants revealed that, rather than UA, allantoin—a byproduct of UA oxidation—was significantly elevated in individuals with dyslipidemia or T2D. Notably, a significant negative correlation was found between serum allantoin level and fasting glucose, as well as serum triglyceride and cholesterol levels. Animal studies demonstrated that allantoin exacerbates hepatic lipid accumulation and glucose intolerance in mice fed a high-fat diet, which was accompanied by increased hepatic lipid biogenesis and reduced bile acid production. Interestingly, our findings indicate that allantoin exhibits a strong binding affinity for PPARα, suggesting that it may act as an inhibitor of PPARα, thereby promoting the progression of MASLD. These results underscore the critical role of allantoin, rather than UA, in the development of MASLD, offering valuable insights for the prediction and management of hepatic metabolic disorders.

2025-06-04 | GSE283505 | GEO

Lymphatic vessels drain monosodium urate and activate immunity in gouty arthritis

Project description:Gouty Arthritis (GA) is caused by urate deposition in the joint capsule, cartilage, bone, and surrounding tissues to trigger recurrent attacks of acute joint inflammation. However, the clearance mechanism of urate deposition is still not clear. We aimed to investigate whether lymphatics vessels can drain monosodium and involve in the immune process of GA. Methods: Inguinal lymph nodes (LNs) in 4 normal volunteers and 4 patients with acute flare of GA were examined by ultrasound. Acute and chronic GA flare mouse models were established by intra-footpad administrations of monosodium urate (MSU) for 1 week or 1 month. Mice were treated with VEGFR-3 inhibitor or undergone popliteal lymph node (PLN) excision or PLN macrophage depletion. The severity of foot inflammation, lymphatic draining function, concentration of uric acid (UA), and macrophage population were examined. Macrophages were co-cultured with MSU-treated lymphatic endothelial cells (LECs) and differential gene expression of LECs was assessed by Agilent gene expression microarray. Results: 1) Draining LNs were enlarged in patients with GA flare and GA mouse models. 2) The lymphatic function and structure were abnormal in GA mouse models. 3) Acute GA mice had elevated UA levels in draining LNs, but not in the serum, while chronic GA mice had elevated UA levels in both LNs and serum. 4) Blockade of VEGFR-3 reduced foot inflammation in chronic GA mice. 5) MSU induces pro-inflammatory polarization of macrophages by inducing LEC inflammation. 6) PLN local depletion of macrophages or removal of PLNs alleviated foot inflammation in GA. Conclusions: Lymphatics drain MSU to the draining LNs to clear deposited urate in the distal extremity and induce LECs to stimulate macrophage pro-inflammatory response during GA. We have identified a novel mechanism about MSU clearance and pro-inflammatory macrophage activation, and provided possible therapeutic approach for GA.

2022-04-02 | GSE199950 | GEO

Transcriptional profiling of Ppr1 gain of function mutant Candida albicans strains

Project description:Metabolic pathways are largely conserved in eukaryotes, but the transcriptional regulation of these pathways can sometimes vary between species; this has been termed rewiring. Recently it has been established that in the Saccharomyces lineage starting from Saccharomyces castelli, genes involved in allantoin breakdown have been genomically relocated to form the DAL cluster. The formation of the DAL cluster occurred along with the loss of urate permease (UAP) and urate oxidase (UOX), reducing the requirement for oxygen and bypassing the candidate Ppr1 inducer, uric acid. In Saccharomyces cerevisiae this allantoin catabolism cluster is regulated by the transcription factor Dal82, which is not present in many of the pre-rearrangement fungal species. We have used ChIP-Chip analysis, transcriptional profiling of an activated Ppr1 protein, bioinformatics, and nitrogen utilization studies, to establish that in Candida albicans the zinc cluster transcription factor Ppr1 controls this allantoin catabolism regulon. Intriguingly, in S. cerevisiae the Ppr1 ortholog binds the same DNA motif (CGG(N6)CCG) as in C. albicans, but serves as a regulator of pyrimidine biosynthesis. This transcription factor rewiring appears to have taken place at the same phylogenetic step as the formation of the rearranged DAL cluster. This transfer of the control of allantoin degradation from Ppr1 to Dal82, together with the repositioning of Ppr1 to the regulation of pyrimidine biosynthesis, may have resulted from a switch to a metabolism that could exploit hypoxic conditions in the lineage leading to S. castellii and S. cerevisiae. 2 samples were analyzed. Cells were grown in YPD media at 30 degrees celcius to OD 0.8. Ppr1 gain of function mutant strain (SCPPR1GAD1A) vs wild type (SC5314) were hybridized, dye swap was done. One replica per array.

2016-04-06 | E-GEOD-79931 | biostudies-arrayexpress

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