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MTA1 Rewires Prostate Cancer Transcriptomes: Direct RNA Interactions Govern Oncogenic Gene Expression and Splice Variant Networks [RIP-Seq]

ABSTRACT: MTA1, a well-characterized epigenetic modifier, plays pivotal roles in cancer progression. However, its involvement in RNA-mediated regulatory mechanisms remains poorly understood. This study unveils MTA1’s dual functionality as a chromatin remodeler and RNA-binding protein (RBP) in prostate cancer (PCa) pathogenesis. By integrating RNA sequencing (RNA-seq) and formaldehyde-crosslinking RNA immunoprecipitation sequencing (fRIP-seq) in PC-3 cells, we demonstrate that MTA1 knockdown dysregulates 1,248 genes and modulates 2,367 alternative splicing events (ASEs). Functional annotation links MTA1-associated differentially expressed genes (DEGs) to extracellular matrix (ECM) remodeling, PI3K-Akt signaling, and hypoxia responses, while ASEs implicate spliceosome activity and RNA processing pathways. fRIP-seq identifies direct MTA1-bound RNAs enriched with GC-rich motifs, with integrative analyses revealing significant overlaps between MTA1 RNA targets and DEGs/ASEs. Our findings establish MTA1 as a multifunctional RBP bridging transcriptional and post-transcriptional networks, offering novel mechanistic insights into PCa progression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE300235 | GEO | 2025/07/01

REPOSITORIES: GEO

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MTA1 Rewires Prostate Cancer Transcriptomes: Direct RNA Interactions Govern Oncogenic Gene Expression and Splice Variant Networks [RNA-Seq]

Project description:MTA1, a well-characterized epigenetic modifier, plays pivotal roles in cancer progression. However, its involvement in RNA-mediated regulatory mechanisms remains poorly understood. This study unveils MTA1’s dual functionality as a chromatin remodeler and RNA-binding protein (RBP) in prostate cancer (PCa) pathogenesis. By integrating RNA sequencing (RNA-seq) and formaldehyde-crosslinking RNA immunoprecipitation sequencing (fRIP-seq) in PC-3 cells, we demonstrate that MTA1 knockdown dysregulates 1,248 genes and modulates 2,367 alternative splicing events (ASEs). Functional annotation links MTA1-associated differentially expressed genes (DEGs) to extracellular matrix (ECM) remodeling, PI3K-Akt signaling, and hypoxia responses, while ASEs implicate spliceosome activity and RNA processing pathways. fRIP-seq identifies direct MTA1-bound RNAs enriched with GC-rich motifs, with integrative analyses revealing significant overlaps between MTA1 RNA targets and DEGs/ASEs. Our findings establish MTA1 as a multifunctional RBP bridging transcriptional and post-transcriptional networks, offering novel mechanistic insights into PCa progression.

2025-07-01 | GSE300236 | GEO

Expression profiling data of Mta1 from E9.0 mouse embryonic fibroblasts

Project description:Mta1 gene expression reveals new targets and functions. Mta1 functions in p53 dependent and independent manner. Genes regulated by Mta1 in the presence and absence of p53 were indetified This expression data contains 5 different samples (MEFs) 1.wild type 2. Mta1 knockout 3. Mta1 re-expression in the knock out MEFs 4. P53 knockout and 5. Mta1 over expression in P53 knock out MEFs. Various sample comparisons were done and genes with p-value< 0.05 and fold change M-bM-^IM-% 2.0 were considered statistically significant 5 samples (triplicates of each, total 15) were analyzed. We generated pairwise comparisons between the WT vs Mta1-KO; Mta1-KO vs Mta1-KO/Mta1; P53-KO vs P53-KO/Mta1.

2013-08-30 | E-GEOD-25072 | biostudies-arrayexpress

MTA1 interacts with primary RNAs to regulate expression and AS by protein dependent manner [CLIP]

Project description:MTA1 is known as its metastatic and invasive function in cancers and the core member of NuRD complex. But the mechanism of regulating gene expression by MTA1 is limited. Besides the interaction with chromosome, MTA1 may play important role at the transcriptional level. We performed co- immunoprecipitation (co-IP) on HCT116 cells and found numerous RNA binding proteins (RBPs), which functions as spliceosome and RNA transport. We then validated that MTA1 interacts with RBPs by RNA dependent manner. By performing the CLIP-seq of MTA1, ten thousands of peaks and thousands of genes were emerged. More detailed analysis and high level of intronic peaks reveal MTA1 prefers to bind pre-mRNAs and regulate the alternative splicing progression by binding the splice site. High overlapping between MTA1 binding and MTA1 regulated genes highlights the direct regulation of RNAs by MTA1 coupling with RBPs. LTK is one of the obvious examples regulated by MTA1. Together, these findings uncover a novel mechanism of MTA1 regulation in transcriptional level as RBPs, and suggest MTA1 regulates pre-mRNA splicing with other RBPs.

2021-01-04 | GSE102634 | GEO

MTA1 interacts with primary RNAs to regulate expression and AS by protein dependent manner [ChIP]

2021-01-04 | GSE102632 | GEO

MTA1 interacts with primary RNAs to regulate expression and AS by protein dependent manner [RNA]

2021-01-04 | GSE102635 | GEO

Expression profiling data of Mta1 from E9.0 mouse embryonic fibroblasts

2013-08-30 | GSE25072 | GEO

Gene expression profiling analysis of nasopharyngeal carcinoma cell CNE1/MTA1-si cells and CNE1 cells

Project description:Investigation of whole genome gene expression level changes in MTA1-silencing CNE1 cells, compared to the wild-type CNE1 cell. A double chip study using total RNA recovered from two cell lines, CNE1/MTA1-si cells and CNE1 cells. Each chip measures the expression level of 45,033 genes from human.

2012-09-14 | E-GEOD-40858 | biostudies-arrayexpress

O-GlcNAc regulates MTA1 transcriptional activity during breast cancer cells genotoxic adaptation

Project description:Chromatin modifier metastatic tumor protein 1 (MTA1), closely correlated with the development and progression in breast cancer, has a fantastic role in multiple cellular processes, including gene expression and cell homeostasis. Although MTA1 is a stress-responsive gene, its role in genotoxic adaptation remains unexplored. Here, we demonstrate that O-GlcNAc modification promotes MTA1 to interact with chromatin and regulates target gene expression, contributing to breast cancer cell genotoxic adaptation. MTA1 is modified with O-GlcNAc residues at serine 237/241/246 in adriamycin adaptive breast cancer cells and that modification improves the genome-wide interactions of MTA1 with gene promotor regions by enhancing its association with nucleosome remodeling and histone deacetylation (NuRD) complex. Further, O-GlcNAc-modulated MTA1 chromatin-binding influences the specific transcriptional regulation of genes involved in the adaptation of breast cancer cells to genotoxic stress. We performed chromatin immunoprecipitation followed by sequencing (ChIP-seq) using anti-HA magnetic beads in HA-MTA1-WT or HA-MTA1-3A stably expressed MCF-7 cells. Next-generation sequencing libraries were generated and amplified for 15 cycles with BGISEQ kit. 100-300 bp DNA fragments were gel-purified and sequenced with BGISEQ-500 (BGI). Two biological replicates of the ChIP-seq were performed. We also analyzed gene expression in MTA1-WT and MTA1-3A expressed cells by RNA-seq.

2020-12-10 | GSE162932 | GEO

NCI-H446 control (NC) and MTA1-overexpressing (OE) cells

Project description:MTA1, SOX4, EZH2 and TGF-β are all potent inducers of epithelial-mesenchymal transition (EMT) in cancer; however, the signaling relationship among these molecules in EMT is poorly understood. Here, we investigated the function of MTA1 in cancer cells and demonstrated that MTA1 overexpression efficiently activates EMT. This activation resulted in a significant increase in the migratory and invasive properties of three different cancer cell lines through a common mechanism involving SOX4 activation, screened from a gene expression profiling analysis. We showed that both SOX4 and MTA1 are induced by TGF-β and both are indispensable for TGF-β-mediated EMT. Further investigation identified that MTA1 acts upstream of SOX4 in the TGF-β pathway, emphasizing a TGF-β-MTA1-SOX4 signaling axis in EMT induction. The histone methyltransferase EZH2, a component of the polycomb (PcG) repressive complex 2 (PRC2), was identified as a critical responsive gene of the TGF-β-MTA1-SOX4 signaling in three different epithelial cancer cell lines, suggesting that this signaling acts broadly in cancer cells in vitro. The MTA1-SOX4-EZH2 signaling cascade was further verified in TCGA pan-cancer patient samples and in a colon cancer cDNA microarray, and activation of genes in this signaling pathway predicted an unfavorable prognosis in colon cancer patients. Collectively, our data uncover a SOX4-dependent EMT-inducing mechanism underlying MTA1-driven cancer metastasis and suggest a widespread TGF-β-MTA1-SOX4-EZH2 signaling axis that drives EMT in various cancers. We propose that this signaling may be used as a common therapeutic target to control epithelial cancer metastasis. We used microarrays to detect MTA1-regulated genes in cancer cells.

2019-10-27 | GSE139429 | GEO

Profiling the target genes for LSD1, MTA1, MTA2, and MTA3 in MCF-7

Project description:Using ChIP-DSL technology from AVIVA SYSTEMS BIOLOGY to find out the whole genome targets for LSD1, MTA1, MTA2, and MTA3 We analyzed arrays using antibodies against LSD1, MTA1, MTA2, or MTA3 and negative control to acquire the enriched ratio of each gene.

2009-08-21 | E-GEOD-14260 | biostudies-arrayexpress

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