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MRNA sequencing SUM159PT WT, Kod and KOs cells cultured in adherent or suspension (i.e. secondary tumorspheres) conditions.

ABSTRACT: mRNA sequencing SUM159PT WT, Kod and KOs cells cultured in adherent or suspension (i.e. secondary tumorspheres) conditions.

PROVIDER: PRJNA472965 | ENA |

REPOSITORIES: ENA

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mRNA sequencing SUM159PT WT, Kod and KOs cells cultured in adherent or suspension (i.e. secondary tumorspheres) conditions.

Project description:The cellular heterogeneity within a tumor can be determined by core genetic and epigenetic programs that operate in certain cells (tumor initiating cells – TICs), providing them with the degree of plasticity needed for induction of metastasis and resistance to therapy. Here we show that the metabolic enzyme nicotinamide N-methyl transferase (NNMT) promotes TIC plasticity in Estrogen Receptor (ER) alpha negative breast cancer. NNMT downregulation delays tumor formation and its full depletion impairs metastasis formation in mice. At the transcriptomic level, NNMT loss results in dowregulation of stem cell and mesenchymal gene signatures, and in the upregulation of luminal features and oxidative metabolism related genes.

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Epigenome analysis of NNMT KO versus WT cells

Project description:Genome wide methylation profiling of SUM159PT NNMT WT, KOs and KOd cells. The Illumina human Infinium Methylation EPIC BeadChip was used to measure global DNA methylation on CpG from 850 k probes. Samples include three experimental replicates from each cell line.

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H3K9me3, H3K27me3, H3K27ac and H3K4me3 ChIP-sequencing in SUM159PT NNMT-WT, NNMT-KOd and NNMT KOs breast cancer cells.

Project description:H3K9me3, H3K27me3, H3K27ac and H3K4me3 ChIP-sequencing in SUM159PT NNMT-WT, NNMT-KOd and NNMT KOs breast cancer cells.

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Project description:The cellular heterogeneity within a tumor can be determined by core genetic and epigenetic programs that operate in certain cells (tumor initiating cells – TICs), providing them with the degree of plasticity needed for induction of metastasis and resistance to therapy. Here we show that the metabolic enzyme nicotinamide N-methyl transferase (NNMT) promotes TIC plasticity in Estrogen Receptor (ER) alpha negative breast cancer. NNMT downregulation delays tumor formation and its full depletion impairs metastasis formation in mice. Mechanistically, NNMT loss increases deposition of H3K9-me2/3 and H3K27-me3 at the promoter of genes involved in stem cell regulation, shutting down their expression and upregulating luminal differentiation genes. This study reveals a major function of NNMT in maintaining core epigenetic programmes that promote TIC self-renewal and metastasis and that repress luminal differentiation.

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Ribosome profiling on SUM159PT cells grown in vitro or in vivo

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