Dataset Information

ChIPseq and RNAseq analysis of T47D cells with/without silencing TRPS1/CHD4

ABSTRACT: We reported the transcriptional regulation function and mechanism of TRPS1-CHD4/NuRD. Overall design: Examination of transcription repression role of TRPS1 in breast cancer cells by ChIP and RNA-seq in duplicates using illumina hiseq2500.

INSTRUMENT(S): Illumina HiSeq 2500 (Homo sapiens)

ORGANISM(S): Homo sapiens

SUBMITTER: liming chen

PROVIDER: GSE114213 | GEO | 2018-12-26

REPOSITORIES: GEO

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Dataset's files

Source:

			Action	DRS
	GSE114213_T47D-TRPS1_peaks.bed.gz	Bed
	GSE114213_T47D_control-CHD4_htcount.txt.gz	Txt
	GSE114213_T47D_control-TRPS1_htcount.txt.gz	Txt
	GSE114213_extractSeq.py.gz	Other

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Publications

Atypical GATA transcription factor TRPS1 represses gene expression by recruiting CHD4/NuRD(MTA2) and suppresses cell migration and invasion by repressing TP63 expression.

Wang Yuzhi Y Lin Xue X Gong Xue X Wu Lele L Zhang Jun J Liu Weiguang W Li Jian J Chen Liming L

Oncogenesis 20181219 12

Transcriptional repressor GATA binding 1 (TRPS1), an atypical GATA transcription factor, functions as a transcriptional repressor and is also implicated in human cancers. However, the underlying mechanism of TRPS1 contributing to malignancy remains obscure. In the current study, we report that TRPS1 recognizes both gene proximal and distal transcription start site (TSS) sequences to repress gene expression. Co-IP mass spectrometry and biochemical studies showed that TRPS1 binds to CHD4/NuRD(MTA2 ...[more]

PMID: 30563971

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Project description:BACKGROUNDS:The NuRD (Nucleosome Remodeling and Deacetylation) complex is a repressive complex in gene transcription by modulating chromatin accessibility of target genes to transcription factors and RNA polymerase II. Although individual subunits of the complex have been implicated in many other cancer types, the complex's role in human hepatocellular carcinoma (HCC) is not fully understood. More importantly, the NuRD complex has not yet been investigated as a whole in cancers. METHODS:We analyzed the expression of the NuRD complex in HCC and evaluated the prognostic value of NuRD complex expression in HCC using the RNA-seq data obtained from the TCGA project. We examined the effect of CHD4 knockdown on HCC cell proliferation, apoptosis, migration, invasion, epithelial-mesenchymal transition, colony-forming ability, and on complement gene expression. We also performed bioinformatic analyses to investigate the correlation between the NuRD complex expression and immune infiltration. RESULTS:We found that nine subunits, out of 14 subunits of the NuRD complex examined, were significantly overexpressed in HCC, and their expression levels were positively correlated with cancer progression. More importantly, our data also demonstrated that these subunits tended to be overexpressed as a whole in HCC. Subsequent studies demonstrated that knockdown of CHD4 in HCC cells inhibits cell proliferation, migration, invasion, and colony-forming ability and promotes apoptosis of HCC cells, indicating that the CHD4/NuRD complex plays oncogenic roles in HCC. Further analysis revealed that the CHD4/NuRD complex regulates complement gene expression in HCC. Intriguingly, we found that the CHD4/NuRD complex expression was inversely correlated with CD8 T cell infiltration in HCC. CONCLUSIONS:Our data demonstrate that the CHD4/NuRD complex plays an oncogenic role in human HCC and regulates complement gene expression in HCC cells. The results of inverse correlation between the CHD4/NuRD complex and CD8 T cell and DC cell infiltration in HCC suggest that the CHD4/NuRD complex not only plays direct regulatory roles in HCC cells, but also has an impact on the immune microenvironment of HCC.