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Identification of RNAs regulated by ZMAT3 and p53

ABSTRACT: Identify the transcriptome regulated by p53 and ZMAT3 in HCT116 colorectal cancer cell line. The hypothsis of this study is that ZMAT3 regulates the expression of a subset of RNAs that are also regulated by p53 to mediate its biological functions.

ORGANISM(S): Homo sapiens

PROVIDER: GSE280756 | GEO | 2025/06/30

REPOSITORIES: GEO

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Identification of RNAs regulated by ZMAT3 and p53

Project description:Identification of RNAs regulated by ZMAT3 and p53

| PRJNA1180478 | ENA

p53-induced RNA-binding protein ZMAT3 is splicing regulator that inhibits the splicing of oncogenic CD44 variants in CRC [RNA-seq_ZMAT3]

Project description:Purpose: p53 is a well-studied protein in which the activation of its main targets is not enough to explain its tumor suppressor effect. Aiming to search for direct p53 targets that mediate less studied processes within p53 pathway, like post-transcriptional regulation, we selected ZMAT3 as the RNA-binding protein most upregulated by p53 activation. Methods: We investigated ZMAT3 targets by using PAR-CLIP and RNA-seq in colorectal cancer cell line HCT116. Results.txt: We found that ZMAT3 binds to ~5000 genes mainly in their introns. It also causes alternative splicing and CD44 was its mostly altered target. ZMAT3 knock-down increased CD44v2-v10 and CD44v3-v10, but decreased CD44s expression. Increased survival and clonogenicity was observed upon knock-down of ZMAT3, which was rescued upon concurrent knock-down of CD44v Conclusions: We propose that ZMAT3 regulates splicing of CD44 following activation by p53, which upregulates CD44s at the expense of CD44v isoforms and leads to a decrease tumorigenicity.

2020-12-18 | GSE150717 | GEO

p53-induced RNA-binding protein ZMAT3 is splicing regulator that inhibits the splicing of oncogenic CD44 variants in CRC [RNA-seq_UPF1]

2020-12-18 | GSE150716 | GEO

p53-induced RNA-binding protein ZMAT3 is splicing regulator that inhibits the splicing of oncogenic CD44 variants in CRC [PAR-CLIP_ZMAT3]

Project description:Purpose: p53 is a well-studied protein in which the activation of its main targets is not enough to explain its tumor suppressor effect. Aiming to search for direct p53 targets that mediate less studied processes within p53 pathway, like post-transcriptional regulation, we selected ZMAT3 as the RNA-binding protein most upregulated by p53 activation. Methods: We investigated ZMAT3 targets by using PAR-CLIP and RNA-seq in colorectal cancer cell line HCT116. Results: We found that ZMAT3 binds to ~5000 genes mainly in their introns. It also causes alternative splicing and CD44 was its mostly altered target. ZMAT3 knock-down increased CD44v2-v10 and CD44v3-v10, but decreased CD44s expression. Increased survival and clonogenicity was observed upon knock-down of ZMAT3, which was rescued upon concurrent knock-down of CD44v Conclusions: We propose that ZMAT3 regulates splicing of CD44 following activation by p53, which upregulates CD44s at the expense of CD44v isoforms and leads to a decrease tumorigenicity.

2020-12-18 | GSE150715 | GEO

Identification of long noncoding RNAs regulated by p53

Project description:Analyize the transcriptpme regulated by p53 in 3 pairs of isogenic p53WT and p53KO colorectal cancer cell lines untreated or treated with Doxorubicin. The hypothsis of this study is that p53 can regulate the expression of subset of lncRNAs to mediate its biological functions.

2017-04-01 | GSE79249 | GEO

Integrative multiomic approaches reveal ZMAT3 and p21 as conserved hubs in the p53 tumor suppression network

Project description:TP53, the most frequently mutated gene in human cancer, encodes a transcriptional activator that induces myriad downstream target genes. Despite the importance of p53 in tumor suppression, the specific p53 target genes important for tumor suppression remain unclear. Recent studies have identified the p53-inducible gene Zmat3 as a critical effector of tumor suppression, but many questions remain regarding its p53-dependence, activity across contexts, and mechanism of tumor suppression alone and in cooperation with other p53-inducible genes. To address these questions, we used Tuba-seqUltra somatic genome editing and tumor barcoding in a mouse lung adenocarcinoma model, combinatorial in vivo CRISPR/Cas9 screens, meta-analyses of gene expression and Cancer Dependency Map data, and integrative RNA-sequencing and shotgun proteomic analyses. We established Zmat3 as a core component of p53-mediated tumor suppression and identified Cdkn1a as the most potent cooperating p53-induced gene in tumor suppression. We discovered that ZMAT3/CDKN1A serve as near-universal effectors of p53-mediated tumor suppression that regulate cell division, migration, and extracellular matrix organization. Accordingly, combined Zmat3-Cdkn1a inactivation dramatically enhanced cell proliferation and migration compared to controls, akin to p53 inactivation. Together, our findings place ZMAT3 and CDKN1A as hubs of a p53-induced gene program that opposes tumorigenesis across various cellular and genetic contexts.

2025-02-21 | GSE289471 | GEO

Identifying Zmat3-bound RNAs

Project description:The goal of the study was to identify RNAs bound by Zmat3 using eCLIP.

2020-11-06 | GSE145555 | GEO

Identifying Zmat3-bound RNAs

Project description:Identifying Zmat3-bound RNAs

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Identification of p53-regulated genes in wild-type p53 or p53-null HCT116 cells

Project description:Identification of p53-regulated genes in wild-type p53 or p53-null HCT116 cells

| PRJNA517505 | ENA

Identification of p53-regulated genes in wild-type p53 or p53-null HCT116 cells

Project description:Microarray-based gene expression analysis of HCT116 p53+/+ and HCT116 p53−/− treated with doxorubicin to activate p53 in time-dependent manner.

2019-01-29 | GSE125787 | GEO

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