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Analysis of DNA methylation in colorectal cancer RKO cells with UHRF1 depletion and HDAC inhibition

ABSTRACT: Analysis of DNA methylation in colorectal cancer RKO cells with UHRF1 depletion and HDAC inhibition

PROVIDER: PRJNA416877 | ENA |

REPOSITORIES: ENA

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Analysis of gene expression in colorectal cancer RKO cells with UHRF1 depletion and HDAC inhibition

Project description:UHRF1 is a major regulator of epigenetic mechanism and is overexpressed in various human malignancies. In this study, we examined the involvement of UHRF1 in aberrant DNA methylation in colorectal cancer (CRC). In CRC cells, transient UHRF1 knockdown rapidly induced DNA demethylation across entire genomic regions, including CpG islands, gene bodies and repetitive elements. Nonetheless, UHRF1 depletion only minimally reversed CpG island hypermethylation-associated gene silencing. However, the combination of UHRF1 depletion and histone deacetylase (HDAC) inhibition synergistically reactivated the silenced genes and strongly suppressed CRC cell proliferation. Our results suggest that (i) maintenance of DNA methylation in CRC cells is highly dependent on UHRF1; (ii) UHRF1 depletion rapidly induces DNA demethylation, though it is insufficient to fully reactivate the silenced genes; and (iii) dual targeting of UHRF1 and HDAC may be an effective new therapeutic strategy.

2019-05-21 | GSE113664 | GEO

Analysis of DNA methylation in colorectal cancer RKO cells with UHRF1 depletion and HDAC inhibition

2019-05-21 | GSE106438 | GEO

Analysis of gene expression in colorectal cancer RKO cells with UHRF1 depletion and HDAC inhibition

Project description:Analysis of gene expression in colorectal cancer RKO cells with UHRF1 depletion and HDAC inhibition

| PRJNA453555 | ENA

Analysis of DNA methylation in colorectal cancer DLD1 cells with UHRF1 depletion and HDAC inhibition

2019-05-21 | GSE106437 | GEO

Analysis of gene expression in colorectal cancer DLD1 cells with UHRF1 depletion and HDAC inhibition

2019-05-21 | GSE106402 | GEO

UHRF1 depletion and HDAC inhibition synergistically reactivate epigenetically silenced genes in colorectal cancer cells

Project description:UHRF1 depletion and HDAC inhibition synergistically reactivate epigenetically silenced genes in colorectal cancer cells

| PRJNA416872 | ENA

Analysis of gene expression in colorectal cancer DLD1 cells with UHRF1 depletion and HDAC inhibition

Project description:Analysis of gene expression in colorectal cancer DLD1 cells with UHRF1 depletion and HDAC inhibition

| PRJNA416773 | ENA

Analysis of DNA methylation in colorectal cancer DLD1 cells with UHRF1 depletion and HDAC inhibition

Project description:Analysis of DNA methylation in colorectal cancer DLD1 cells with UHRF1 depletion and HDAC inhibition

| PRJNA416878 | ENA

UHRF1 depletion and HDAC inhibition reactivate epigenetically silenced genes in colorectal cancer cells.

Project description: Not available

| S-EPMC6505222 | biostudies-literature

Tumor-promoting functions of UHRF1 in retinoblastoma

Project description:UHRF1 (ubiquitin-like with PHD and ring finger domains 1) is an epigenetic regulator that is involved in the regulation of DNA and histone methylation and many other cellular events. The UHRF1 is frequently found to be overexpressed in various human cancers including retinoblastoma, and its overexpression has been associated with tumor-promoting effects such as inhibition of apoptosis and high metastatic potential. However, the detailed mechanisms underlying these tumor-promoting functions of UHRF1 in retinoblastoma still remain unclear. In this study, we uncovered that UHRF1 depletion in retinoblastoma cells sensitizes the cells to histone deacetylase (HDAC) inhibitors, augmenting apoptotic cell death. To understand the molecular mechanisms underlying the enhanced sensitivity to HDAC inhibitors in the UHRF1-depleted retinoblastoma cells, we performed the gene expression profiling in UHRF1-knockdown Y79 cells in comparison with control-knockdown cells by RNA-sequencing to identify differentially expressed genes. Our RNA-seq results revealed that UHRF1 depletion downregulates redox-responsive genes such as GSTA4 and TXN2, leading to increased intracellular oxidative stress and higher susceptibility to HDAC inhibitor treatment.

2020-02-10 | GSE135424 | GEO

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