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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE102634 | GEO | 2021/01/04

REPOSITORIES: GEO

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

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 | GSE102632 | GEO

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

2021-01-04 | GSE102635 | GEO

RNA-binding chromatin modifier MTA1 regulates mitotic transition and tumorigenesis by orchestrating mitotic mRNA processing [fCLIP-Seq]

Project description:The processing of RNAs by chromatin-associated proteins (CAPs) is highlighted by the latest findings. However, whether and how CAP-RNA interactions regulate cancer biology remain underdefined. Using modified fCLIP-seq technology, we show that, cancer metastasis-associated antigen 1 (MTA1), a well-known oncogenic chromatin modifier, binds bulk transcripts, preferentially at splicing-responsible motifs, influencing the abundance and alternative splicing (AS) of target transcripts, preferentially those encoding mitosis regulators. MTA1 orchestrates the fluctuant pre-mRNA AS kinetics of mitosis regulators, such as ATRX and MYBL2, during mitosis. MTA1 overexpression causes a defective mitotic arrest, leading to aberrant chromosome segregation, and CIN occurrence in cancer cells and clinical tumors, which eventually contributes to tumorigenesis. Hence, we present MTA1 as a pivotal RNA-binding CAP linked to mitosis control in tumorigenesis.

2020-07-17 | GSE123956 | GEO

RNA-binding chromatin modifier MTA1 regulates mitotic transition and tumorigenesis by orchestrating mitotic mRNA processing [ChIP-Seq]

2020-07-17 | GSE123955 | GEO

RNA-binding chromatin modifier MTA1 regulates mitotic transition and tumorigenesis by orchestrating mitotic mRNA processing [Synchronized RNA-seq]

2020-07-17 | GSE123958 | GEO

RNA-binding chromatin modifier MTA1 regulates mitotic transition and tumorigenesis by orchestrating mitotic mRNA processing [Non-synchronized RNA-seq]

2020-07-17 | GSE123957 | 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

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

Human colon cancer HCT116 cell LC/MSMS

Project description:Mitosis deregulation is a key event during carcinogenesis. Alternative splicing spectrum alteration plays a critical role during mitosis shift. However, the molecules responsible for dysregulated alternative splicing driving carcinogenetic mitosis remain poorly defined. Here, we demonstrate that cancer metastasis-associated antigen 1 (MTA1), a well-known oncogenic chromatin modifier, broadly interacts and co-expresses with RBPs across cancers, contributes to cancerous mitosis-related alternative splicing. Using developed fCLIP-seq technology, we show that MTA1 binds abundant transcripts, preferentially at splicing-responsible motifs, influencing both the abundance and alternative splicing (AS) of target transcripts. MTA1 is cytoplasmic and extrachromosomal at mitosis. Through the RNA-association activity, MTA1 regulates the mRNA level and guides the AS of a serious of mitosis regulators to control the mitosis. MTA1 deletion abrogated the dynamic AS switches of variants for ATRX and MYBL2 at mitotic stage, which are relevant to mitosis and tumorigenesis. MTA1 dysfunction causes a defective mitotic arrest, leading to aberrant chromosome segregation, and resultantly chromosomal instability (CIN) in cancer cells and tissues, which eventually contributes to tumorigenesis. Currently, little is known about the RNA splicing during mitosis, here, we present MTA1 as a pivotal RNA-binding protein, functioning to orchestrate the dynamic splicing of mitosis regulators linked to mitosis control in tumorigenesis.

2020-03-30 | PXD018242 | iProX

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

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