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ZMAT2 condensates regulate the alternative splicing of TRIM28 to promote the proliferation of hepatocellular carcinoma cells

ABSTRACT: ZMAT2 condensates regulate the alternative splicing of TRIM28 to promote the proliferation of hepatocellular carcinoma cells

PROVIDER: PRJNA1099274 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28637100_1.fastq.gz	Fastqsanger.gz
	SRR28637100_2.fastq.gz	Fastqsanger.gz
	SRR28637101_1.fastq.gz	Fastqsanger.gz
	SRR28637101_2.fastq.gz	Fastqsanger.gz

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ZMAT2 condensates regulate the alternative splicing of TRIM28 to promote the proliferation of hepatocellular carcinoma cells

Project description:Dysregulation of splicing factor expression plays a crucial role in the progression of hepatocellular carcinoma (HCC). Our research found that the expression level of splicing factor ZMAT2 is increased in HCC, promoting the proliferation of hepatocellular carcinoma cells. RNA-seq data indicated that ZMAT2 regulated exon skipping of mRNA, while RIP-seq data further revealed the binding motifs of ZMAT2. A comprehensive analysis of RNA-seq and RIP-seq data indicateed that ZMAT2 plays a crucial role in the maturation process of TRIM28 mRNA. Deletion of ZMAT2 led to the deletion of 25 bases in exon 11 of TRIM28, ultimately resulting in nonsense-mediated decay (NMD). Previous studies have demonstrated a close association between TRIM28 and the proliferation of hepatocellular carcinoma. Our experiments have revealed that TRIM28 serves as a critical factor for ZMAT2 in facilitating the proliferative process of hepatocellular carcinoma. Studies have demonstrated a close correlation between the mRNA splicing process and the occurrence of phase separation. Our research discovered that ZMAT2 is capable of undergoing phase separation, resulting in the formation of liquid droplet condensates within hepatocellular carcinoma cells. Additionally, it was found that ZMAT2 is able to form protein-nucleic acid condensates with TRIM28 mRNA. In summary, we hypothesize that ZMAT2 and TRIM28 mRNA form protein-nucleic acid condensates, thereby regulating the splicing of TRIM28 mRNA. The augmented expression of ZMAT2 in hepatocellular carcinoma cells results in the upregulation of TRIM28 expression, ultimately driving the proliferation of hepatocellular carcinoma cells.

2024-07-16 | GSE263805 | GEO

ZMAT2 condensates regulate the alternative splicing of TRIM28 to promote the proliferation of hepatocellular carcinoma cells

2024-07-09 | GSE263501 | GEO

ZMAT2 condensates regulate the alternative splicing of TRIM28 to promote the proliferation of hepatocellular carcinoma cells

Project description:ZMAT2 condensates regulate the alternative splicing of TRIM28 to promote the proliferation of hepatocellular carcinoma cells

| PRJNA1097652 | ENA

Hijacking of transcriptional condensates by endogenous retroviruses

Project description:Heterochromatin plays essential roles in repressing retrotransposons, e.g. endogenous retroviruses (ERVs) during mammalian development, but the contribution of retrotransposition to lethality observed in embryonic cells deficient for heterochromatin-mediated ERV repression is poorly understood. Here we report that selective degradation of the TRIM28 heterochromatin adapter protein leads to reduced association of transcriptional condensates with loci encoding super-enhancer -driven pluripotency genes in embryonic stem cells, a collapse of the pluripotency transcriptional circuit, and a pre-lethal restriction of pluripotent lineages in mouse embryos. De-repressed ERVs recruit transcriptional condensates in the absence of TRIM28, and ERV RNA facilitates condensation of RNA Polymerase II in vitro. We propose that retrotransposons contribute to the genomic distribution of nuclear condensates, and that RNA species may facilitate “hijacking” of transcriptional condensates in various developmental and disease contexts.

2022-07-08 | PXD021895 | Pride

Hijacking of transcriptional condensates by endogenous retroviruses

Project description:Most endogenous retroviruses (ERVs) in mammals are incapable of retrotransposition; therefore, why ERV de-repression is associated with lethality during early development has been a mystery. Here we report that rapid and selective degradation of the TRIM28 heterochromatin adapter protein triggers dissociation of transcriptional condensates from loci encoding super-enhancer -driven pluripotency genes, and their association with transcribed ERV loci in murine embryonic stem cells. Knockdown of ERV RNAs or forced expression of super-enhancer -enriched transcription factors rescued condensate localization at super-enhancers in TRIM28-degraded cells. In a biochemical reconstitution system, ERV RNA facilitated partitioning of RNA Polymerase II, and the Mediator co- activator into phase-separated droplets. In TRIM28 knockout mouse embryos, single-cell RNA-Seq analysis revealed specific depletion of pluripotent lineages. We propose that coding and non-coding nascent RNAs, including those produced by retrotransposons, may facilitate “hijacking” of transcriptional condensates in various developmental and disease contexts.

2022-03-30 | GSE159468 | GEO

ZMAT2 condensates regulate the alternative splicing of TRIM28 to reduce cellular ROS accumulation, thereby promoting the proliferation of HCC cells

Project description: Not available

| S-EPMC11337747 | biostudies-literature

TRIM28 interacts with EZH2 and SWI/SNF to activate genes that promote mammosphere formation

Project description:EZH2 is generally associated with H3K27 methylation and gene silencing. Mass spectrometry of the EZH2-interactome in MCF7 cells revealed EZH2-interactions with SWI/SNF subunits and TRIM28, which formed a complex with EZH2 distinct from PRC2. Transcriptome profiling showed that EZH2 primarily activates transcription in MCF7 cells and with TRIM28 co-regulates a set of genes associated with stem cell maintenance and poor survival of breast cancer patients. TRIM28 depletion repressed EZH2 recruitment and expression of this gene set, in parallel with decreased CD44hi/CD24lo mammosphere formation. These results support PRC2-independent functions of EZH2 and TRIM28 in mammary stem cell enrichment and maintenance.

2017-07-18 | GSE76271 | GEO

Phosphorylation regulates viral biomolecular condensates to promote infectious progeny production

Project description:Biomolecular condensates play important roles in diverse biological processes. Many viruses form biomolecular condensates which have been implicated in various functions critical for productive infection of host cells. The adenovirus L1-52/55 kilodalton protein (52K) was recently shown to form viral biomolecular condensates that coordinate viral genome packaging and capsid assembly. Although critical for packaging, we do not know how viral condensates are regulated during adenovirus infection. Here we show that phosphorylation of serine residues 28 and 75 within the N-terminal intrinsically disordered region of 52K modulates viral condensates in vitro and in cells, promoting liquid-like properties over condensate hardening. Furthermore, we demonstrate that phosphorylation of 52K promotes viral genome packaging and production of infectious progeny particles. Collectively, our findings provide insights into how viral condensate properties are regulated and maintained in a state conducive to their function in viral progeny production. In addition, our findings have implications for antiviral strategies aimed at targeting the regulation of viral biomolecular condensates to limit viral multiplication.

2023-12-06 | PXD046971 | Pride

TRIM28 is essential for erythroblast differentiation in the mouse

Project description:We discovered that Trim28 genetic loss in the adult mouse leads to defective immature erythropoiesis in the bone marrow and consequently to anemia.We further found that TRIM28 controls erythropoiesis in a cell-autonomous manner by inducibly deleting Trim28 exclusively in hematopoietic cells. Finally, in the absence of TRIM28 we observed increased apoptosis as well as diminished expression of multiple erythroid transcription factors and heme biosynthetic enzymes in immature erythroid cells. Thus, TRIM28 is essential for the cell-autonomous development of immature erythroblasts in the bone marrow. To induce Cre recombinase from the Mx1Cre transgene, poly(I:C) was injected 5 times every other day. Mice were analyzed two weeks after completion of poly(I:C) administration. TRIM28 mutant mice generate two distinct types of immature erythroid cells; KOa, with 5-8% of the Trim28 gene remaining undeleted (still bearing 26% of residual mRNA), and KOb, with 1-4% of the gene remaining undeleted (and with 18% of mRNA remaining).

2013-10-04 | E-GEOD-49843 | biostudies-arrayexpress

Transcription profiling of human primary bronchial/tracheal epithelial cells treated with 10 different sources of cigarette smoke condensates

Project description:Nine cigarette smoke condensates (CSCs) were produced under a standard ISO smoking machine regimen and one was produced by a more intense smoking machine regimen. These CSCs were used to treat primary normal human bronchial epithelial cells for 18 hours. Experiment Overall Design: Primary human bronchial/tracheal epithelial cells were grown in culture and treated with 10 different sources of cigarette smoke condensates.

2009-10-03 | E-GEOD-18235 | biostudies-arrayexpress

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