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Non-enzymatic SETD1A activity drives breast cancer cell proliferation via cyclin K. (ChIP-seq)

ABSTRACT: Non-enzymatic SETD1A activity drives breast cancer cell proliferation via cyclin K. (ChIP-seq)

PROVIDER: PRJNA1222328 | ENA |

REPOSITORIES: ENA

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Non-enzymatic SETD1A activity drives breast cancer cell proliferation via cyclin K.

Project description:Non-enzymatic SETD1A activity drives breast cancer cell proliferation via cyclin K.

| PRJNA1222325 | ENA

Non-enzymatic SETD1A activity drives breast cancer cell proliferation via cyclin K. (RNA-seq)

Project description:Non-enzymatic SETD1A activity drives breast cancer cell proliferation via cyclin K. (RNA-seq)

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Non-enzymatic SETD1A activity drives breast cancer cell proliferation via cyclin K. (RNA-seq)

Project description:Breast cancer is the most common cancer in women worldwide. SETD1A, a histone H3 lysine-4 methyltransferase, is associated with poor prognosis in breast cancer. While both its enzymatic and non-enzymatic functions have been implicated in cancer progression, the specific role of SETD1A in breast cancer remains unclear. This study aimed to elucidate the molecular mechanisms underlying SETD1A dependency in breast cancer.

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Non-enzymatic SETD1A activity drives breast cancer cell proliferation via cyclin K. (ChIP-seq)

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A non-catalytic function of SETD1A regulates Cyclin K and the DNA damage response [RNA-seq]

Project description:MLL/SET methyltransferases catalyze methylation of histone 3 lysine 4 and play critical roles in development and cancer. We assessed MLL/SET proteins and found that SETD1A is required for survival of acute myeloid leukemia (AML) cells. Mutagenesis studies and CRISPR-Cas9 domain screening, showed the enzymatic SET domain is not necessary for AML cell survival but that a newly identified region, termed the FLOS (Functional Location on SETD1A) domain, is indispensable. FLOS disruption suppresses DNA damage response genes and induces p53-dependent apoptosis. The FLOS domain acts as a Cyclin K-binding site that is required for chromosomal recruitment of Cyclin K, and for DNA repair-associated gene expression in S phase. These data identify a connection between the chromatin regulator SETD1A and the DNA damage response that is independent of histone methylation, and suggests that targeting SETD1A and Cyclin K complexes may represent a therapeutic opportunity for AML and potentially other cancers.

2018-02-01 | GSE108614 | GEO

SETD1A regulates transcriptional pause release of heme biosynthesis genes in leukemia [RNA-seq]

Project description:Histone methyltransferase SETD1A is critical for acute myeloid leukemia (AML) cell survival, but the molecular mechanism driving SETD1A gene regulation remains elusive. To delineate the role of SETD1A, we utilize a protein degrader technology to induce rapid SETD1A degradation in AML cell lines. SETD1A degradation results in immediate downregulation of transcripts associated with DNA repair and heme biosynthesis pathways. CRISPR-based functional analyses and metabolomics revealed an essential role of SETD1A to maintain mitochondrial respiration in AML cells. These SETD1A targets are enriched in head-to-head (H2H) genes. SETD1A degradation disturbs a non-enzymatic SETD1A domain-dependent cyclin K function, increases the mono-Ser5P RNA polymerase II (RNAP2) at TSS, and induces the promoter-proximal pausing of RNAP2 in a strand-specific manner. This study reveals a non-enzymatic role for SETD1A in transcriptional pause release and provides insight into the mechanism of RNAP2 pausing and its function in cancer.

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SETD1A regulates transcriptional pause release of heme biosynthesis genes in leukemia [ChIP-Seq]

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Non-enzymatic SETD1A activity drives breast cancer cell proliferation via cyclin K.

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-08-07 | GSE289278 | GEO

SETD1A function is mediated through interaction with mitotic regulators BuGZ/BUB3 in leukemia [RNA-seq]

Project description:The H3K4 methyltransferase SETD1A plays a crucial role in leukemia cell survival through its non-catalytic FLOS domain mediated recruitment of cyclin K and regulation of DNA damage response genes. In this study, we identify a functional nuclear localization signal and interaction partners for the FLOS domain. Our proteomics analysis against FLOS domain-binding partners reveals that the SETD1A FLOS domain binds mitosis-associated proteins BuGZ/BUB3. Targeted inhibition of both cyclin K and BuGZ/BUB3 binding motifs on SETD1A shows synergistic anti-leukemic effects. BuGZ/BUB3 localize to SETD1A-positive promoter-TSS regions and SETD1A-negative H3K4me1-positive enhancer regions adjacent to SETD1A-target genes. The GLEBS motif and intrinsically disordered region of BuGZ are required for both SETD1A binding and the leukemia cell proliferation. Despite the role of BuGZ/BUB3 at mitotic phase, the cell-cycle specific SETD1A restoration study indicates the roles of SETD1A at G1/S phase of cell cycle. Discovery of this complex indicates the indispensable role of the SETD1A-BuGZ axis in cancer.

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SETD1A function is mediated through interaction with mitotic regulators BuGZ/BUB3 in leukemia [ChIP-seq]

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