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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE106439 | GEO | 2019/05/21

REPOSITORIES: GEO

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

Project description: Not available

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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

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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.

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HeLa TI cell-based assay as a new approach to screen for chemicals able to reactivate the expression of epigenetically silenced genes.

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Targeting CDK9 Reactivates Epigenetically Silenced Genes in Cancer.

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Targeting CDK9 Reactivates Epigenetically Silenced Genes in Cancer

Project description:Cyclin-Dependent Kinase 9 (CDK9) as part of the PTEFb complex promotes transcriptional elongation by promoting RNAPII pause release. We now report that, paradoxically, CDK9 is also essential for maintaining gene silencing at heterochromatic loci. Through a live cell screen, we discovered that CDK9 inhibition reactivates epigenetically silenced genes in cancer, leading to restored tumor suppressor gene expression and cell differentiation, along with activation of endogenous retrovirus (ERV) genes. CDK9 inhibition dephosphorylates the SWI/SNF protein SMARCA4 and represses HP1α expression, both of which contribute to gene reactivation. Based on gene activation, we developed the highly selective and potent CDK9 inhibitor MC180295 (IC50 =5.1nM) that has broad anti-cancer activity in-vitro and is effective in in-vivo cancer models. Additionally, CDK9 inhibition sensitizes with the immune checkpoint inhibitor α-PD-1 in vivo, making it an excellent target for epigenetic therapy of cancer.

2020-05-26 | PXD007925 | Pride

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