Elucidating the mechanisms underlying H3K18la contributes to NSCLC progression
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE245990 | GEO | 2024/08/06
REPOSITORIES: GEO
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Project description:L-lactate was reported as a precursor that can label and stimulate histone lysine-N-L-lactylation (Kla), which represents a new epigenetic mark affecting gene expression directly via histone PTMs under conditions of high glycolysis, such as the Warburg effect. To investigate the genome-wide targeting of H3K18la, we performed ChIP-seq in H1299 cells using anti-H3K18la antibody. 50.6% of the H3K18la binding sites displayed enrichment close to -1kb promoter of genes. More importantly, our ChIP-seq data showed that H3K18la is enriched in many genes that related with replication processes, highlighted the importance of histone Kla involved in DNA replication.
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Project description:We profiled the genome-wide distribution of H3K18la in samples originating from 6 different in vitro and in vivo mouse samples, representing 3 tissues: embryonic stem cells, macrophages and skeletal muscle as well as in human skeletal muscle and compared them to the profiles of other well-established histone modifications as well as gene expression patterns. Globally, we found that H3K18la profiles resemble H3K27ac profiles better than any other investigated hPTM, including H3K4me3, but that they do not copy them. For all samples, H3K18la marked active CGI promoters of highly expressed genes which were remarkably shared across the different mouse tissues and which contained many housekeeping genes. Promoter H3K18la levels correlated positively to both H3K27ac and H3K4me3 levels as well as to gene expression levels. In addition, we found that H3K18la is enriched at tissue-type specific, active enhancers, which are particularly tissue-type-specific, especially when compared to the H3K18la-marked promoter regions. Accordingly, enhancer H3K18la levels correlate positively to the expression of their nearest genes. Additionally, genes closest to enhancers with high H3K18la levels predominantly consist of tissue-type specific marker genes. Overall, we showed that H3K18la is not only a marker for active promoters, but that it also marks active enhancers, and this both in embryonic tissues and differentiated tissues, and both in mouse and in human.
2022-09-14 | GSE195859 | GEO
Project description:We profiled the genome-wide distribution of H3K18la in samples originating from 6 different in vitro and in vivo mouse samples, representing 3 tissues: embryonic stem cells, macrophages and skeletal muscle as well as in human skeletal muscle and compared them to the profiles of other well-established histone modifications as well as gene expression patterns. Globally, we found that H3K18la profiles resemble H3K27ac profiles better than any other investigated hPTM, including H3K4me3, but that they do not copy them. For all samples, H3K18la marked active CGI promoters of highly expressed genes which were remarkably shared across the different mouse tissues and which contained many housekeeping genes. Promoter H3K18la levels correlated positively to both H3K27ac and H3K4me3 levels as well as to gene expression levels. In addition, we found that H3K18la is enriched at tissue-type specific, active enhancers, which are particularly tissue-type-specific, especially when compared to the H3K18la-marked promoter regions. Accordingly, enhancer H3K18la levels correlate positively to the expression of their nearest genes. Additionally, genes closest to enhancers with high H3K18la levels predominantly consist of tissue-type specific marker genes. Overall, we showed that H3K18la is not only a marker for active promoters, but that it also marks active enhancers, and this both in embryonic tissues and differentiated tissues, and both in mouse and in human.
2022-09-14 | GSE195854 | GEO
Project description:We profiled the genome-wide distribution of H3K18la in samples originating from 6 different in vitro and in vivo mouse samples, representing 3 tissues: embryonic stem cells, macrophages and skeletal muscle as well as in human skeletal muscle and compared them to the profiles of other well-established histone modifications as well as gene expression patterns. Globally, we found that H3K18la profiles resemble H3K27ac profiles better than any other investigated hPTM, including H3K4me3, but that they do not copy them. For all samples, H3K18la marked active CGI promoters of highly expressed genes which were remarkably shared across the different mouse tissues and which contained many housekeeping genes. Promoter H3K18la levels correlated positively to both H3K27ac and H3K4me3 levels as well as to gene expression levels. In addition, we found that H3K18la is enriched at tissue-type specific, active enhancers, which are particularly tissue-type-specific, especially when compared to the H3K18la-marked promoter regions. Accordingly, enhancer H3K18la levels correlate positively to the expression of their nearest genes. Additionally, genes closest to enhancers with high H3K18la levels predominantly consist of tissue-type specific marker genes. Overall, we showed that H3K18la is not only a marker for active promoters, but that it also marks active enhancers, and this both in embryonic tissues and differentiated tissues, and both in mouse and in human.
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Project description:Tumor cells are known for excessive lactate production, due to Warburg effect, and transcriptional dysregulation. However, how lactate influences the epigenetic modifications at a genome-wide level and its impact on gene transcription in tumor cell remains unclear. Addressing this gap, we analyzed genome-wide modification of H3K18 lactylation (H3K18la) in T-cell acute lymphoblastic leukemia (T-ALL). Integrated analysis with histone modifications with established functions show the H3K18la is mainly involved in active regulation of gene transcription. We report increased lactate and H3K18la modification levels in T-ALL as compared to normal T cells. We observe clusters of H3K18la modifications in patterns reminiscent of super-enhancers. We show a notable shift of genome-wide H3K18la modification from T cell immunity in normal T cells to leukemogenesis in T-ALL, correlating with altered gene transcription profiles. By disrupting H3K18la modification, we uncover both synergetic and divergent changes between H3K18la and H3K27ac modifications, suggesting the H3K18la and H3K27ac modifications may have specific regulation mechanisms correspondingly. These findings expand our understanding of metabolic disruptions involvement in transcription dysregulation through epigenetic changes in T-ALL, and emphasize the collective importance of histone modifications in maintaining oncogenic epigenetic stability.
2024-05-20 | GSE263697 | GEO
Project description:Tumor cells are known for excessive lactate production, due to Warburg effect, and transcriptional dysregulation. However, how lactate influences the epigenetic modifications at a genome-wide level and its impact on gene transcription in tumor cell remains unclear. Addressing this gap, we analyzed genome-wide modification of H3K18 lactylation (H3K18la) in T-cell acute lymphoblastic leukemia (T-ALL). Integrated analysis with histone modifications with established functions show the H3K18la is mainly involved in active regulation of gene transcription. We report increased lactate and H3K18la modification levels in T-ALL as compared to normal T cells. We observe clusters of H3K18la modifications in patterns reminiscent of super-enhancers. We show a notable shift of genome-wide H3K18la modification from T cell immunity in normal T cells to leukemogenesis in T-ALL, correlating with altered gene transcription profiles. By disrupting H3K18la modification, we uncover both synergetic and divergent changes between H3K18la and H3K27ac modifications, suggesting the H3K18la and H3K27ac modifications may have specific regulation mechanisms correspondingly. These findings expand our understanding of metabolic disruptions involvement in transcription dysregulation through epigenetic changes in T-ALL, and emphasize the collective importance of histone modifications in maintaining oncogenic epigenetic stability.
2024-05-31 | GSE263584 | GEO
Project description:After injury, muscles require fully functional macrophages to recover completely. During muscle regeneration, macrophages transition from a pro-inflammatory to a pro-restorative phenotype ensures the proper regeneration. Lactate is a crucial molecule for muscle-residing macrophage polarisation. Histone lactylation, a direct derivative of lactate, has been implicated in macrophage polarisation in vitro . In this work, we show for the first time that macrophages recruited to the muscle after ischemic injury modify their histone lactylome between 2 and 4 days post injury. Absolute histone lactylation levels increase significantly. Although subtly, also the genomic enrichment of H3K18la changes from 2 to 4 days post injury and this correlates with gene expression changes. Interestingly, we find that H3K18la genomic enrichment changes from day 2 to day 4 post injury are predictive for gene expression changes later in time, from day 4 to day 7, rather than being a reflection of past gene expression changes from day 1 to day 2. Our results suggest that histone lactylation dynamics are functionally important for the resolving action of macrophages during muscle regeneration.
2024-04-08 | GSE254129 | GEO