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H3K9 dimethylation safeguards cancer cells against activation of the Interferon pathway

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE160532 | GEO | 2022/03/18

REPOSITORIES: GEO

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H3K9 dimethylation safeguards cancer cells against activation of the Interferon pathway [WGBS]

Project description:Activation of interferon genes constitutes an important anticancer pathway able to restrict proliferation of cancer cells. Here we demonstrate that the H3K9me3 histone methyl transferase (HMT) Suppressor of Variegation 3-9 Homolog 1 (SUV39H1) is required for the proliferation of Acute Myeloid Leukemia (AML) and find that its loss leads to activation of the interferon pathway. Mechanistically, we show that this occurs via destabilization of a complex composed of SUV39H1 and the two H3K9me2 HMTs, G9A and GLP. Indeed, loss of H3K9me2 correlated with the activation of key interferon pathway genes, and interference with the activities of G9A/GLP largely phenocopied loss of SUV39H1. Finally, we demonstrate that inhibition of G9A/GLP synergized with DNA demethylating agents and that SUV39H1 constitutes a potential biomarker for the response to hypomethylation treatment. Collectively, we uncovered a clinically relevant role for H3K9me2 in safeguarding cancer cells against activation of the interferon pathway.

2022-03-18 | GSE182056 | GEO

H3K9 dimethylation safeguards cancer cells against activation of the Interferon pathway [SUV39H1_ChIP-seq]

Project description:Activation of the interferon genes constitutes an important anticancer pathway, able to restrict proliferation of cancer cells. Here we demonstrate that the H3K9me3 histone methyl transferase (HMT) Suppressor Of Variegation 3-9 Homolog 1 (SUV39H1) is required for the proliferation of Acute Myeloid Leukemia (AML) and find that its loss leads to activation of the interferon pathway. Mechanistically, we show that this occur via destabilization of a complex composed of SUV39H1 and the two H3K9me2 HMTs G9a and GLP. Indeed, loss of H3K9me2 correlated with the activation of key interferon pathway genes and interference with the activities of G9a/GLP largely phenocopied loss of SUV39H1. Finally, we demonstrated that inhibition of G9a/GLP synergized with DNA demethylating agents and that SUV39H1 constitutes a potential biomarker the response to hypomethylation treatment. Collectively, we uncovered a clinical relevant role for H3K9me2 in safeguarding cancer cells against activation of the interferon pathway.

2022-03-18 | GSE190469 | GEO