RNA-seq of cells with TET1 knockout
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA475531 | ENA |
REPOSITORIES: ENA
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Project description:TET1 oxidizes methylated cytosine into 5-hydroxymethylcytosine, resulting in regulation of DNA methylation and gene expression. Full length TET1 (TET1-FL) has a CXXC domain that binds to unmethylated stretches of CpG dinucleotides known as CpG islands (CGIs). This CXXC domain allows TET1 to protect CGIs from aberrant methylation but it also limits its ability to regulate genes outside of CGIs. Here we report a novel isoform of TET1 (TET1-ALT) that has a unique transcription start site from an alternate promoter in intron 2, yielding a protein with a unique translation start site. Importantly, TET1-ALT lacks the CXXC domain but retains the catalytic domain. To identify the gene expression targets of TET1-ALT and to compare them to the gene expression targets of TET1-FL, we performed RNA-seq on HEK293T cells that overexpress either Empty Vector (Control), TET1-FL or TET1-ALT.
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Project description:Both gains and losses of DNA methylation are common in cancer but the factors controlling this methylation balance remain unclear. Triple negative breast cancer (TNBC), a subtype that does not overexpress hormone receptors or HER2/NEU is one of the most hypomethylated cancers observed. In search for an explanation for this, we discovered that the TET1 DNA demethylase is specifically overexpressed in about 40% of patients with TNBC, where it is associated with hypomethylation of up to 10% of queried CpG sites and a worse overall survival. Through bioinformatic analyses in both breast and ovarian cancer cell line panels, we uncovered an intricate network connecting TET1 to hypomethylation and activation of cancer specific oncogenic pathways including PI3K, EGFR and PDGF. TET1 expression correlated with sensitivity to drugs targeting the PI3K-mTOR pathway. CRISPR mediated deletion of TET1 in two independent TNBC cell lines resulted in reduced expression of PI3K pathway genes, upregulation of immune response genes and substantially reduced cellular proliferation, suggesting dependence of oncogenic pathways on TET1 overexpression. Our work establishes TET1 as a potential oncogene that contributes to aberrant hypomethylation in cancer and suggests that TET1 could serve as a novel druggable target for therapeutic intervention.
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Project description:DNA hypermethylation is known to contribute to the formation of cancer. However, DNA hypomethylation has received far less attention and the factors controlling the balance between hypo and hypermethylation and its impact on tumorigenesis remains unclear. Triple negative breast cancer (TNBC), a subtype of breast cancer that does not overexpress the hormone receptors or HER2/NEU, is one of the most hypomethylated cancers observed. Importantly, TNBCs are often a therapeutic challenge because of advanced presentation and lack of targeted therapies. TET1 is a DNA demethylase that regulates DNA methylation, hydroxymethylation and gene expression. We found that TET1 is specifically overexpressed in TNBC, where it is associated with hypomethylation and a worse overall survival. Further, we uncover an intricate network connecting TET1 expression to maintaining activation of cancer specific pathways, including PI3K, EGFR and PDGF. In TET1 KO cells, we observed reduced phospho-4EBP1 and decreased expression of genes in the PI3K pathway, suggesting loss of PI3K-mTOR activity is concomitant with loss of TET1. Additionally, TET1 KO cells have reduced cellular proliferation and migration. Our work establishes TET1 as an oncogene that contributes to the aberrant hypomethylation observed in cancer and suggests TET1 could serve as a novel druggable target for therapeutic intervention.
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Study Design: historical control
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