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The diapause-like colorectal cancer cells induced by SMC4 attenuation are characterized by low proliferation and chemotherapy insensitivity [CUT&TAG]

ABSTRACT: CUT-Tag for histone H4K12la in HCT116 cells and its shSMC4.

ORGANISM(S): Homo sapiens

PROVIDER: GSE208202 | GEO | 2022/07/17

REPOSITORIES: GEO

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The diapause-like colorectal cancer cells induced by SMC4 attenuation are characterized by low proliferation and chemotherapy insensitivity [ATAC-seq]

Project description:ATAC-seq for HCT116 cells and its shSMC4.

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The diapause-like colorectal cancer cells induced by SMC4 attenuation are characterized by low proliferation and chemotherapy insensitivity [RNA-seq]

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The diapause-like colorectal cancer cells induced by SMC4 attenuation are characterized by low proliferation and chemotherapy insensitivity [CUT&TAG]

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Colorectal cancer cells with Suppressed SMC4 display a diapause-like state showing slow proliferation and chemotherapy insensitivity

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

2022-07-17 | GSE208204 | GEO

The diapause-like colorectal cancer cells induced by SMC4 attenuation are characterized by low proliferation and chemotherapy insensitivity [ATAC-seq]

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Project description:The diapause-like colorectal cancer cells induced by SMC4 attenuation are characterized by low proliferation and chemotherapy insensitivity[scRNA-seq]

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PFKFB3 drives renal fibrosis through promoting histone lactylation-mediated NF- B activation [CUT&Tag]

Project description:Persistently elevated glycolysis in kidney has been demonstrated to promote chronic kidney disease. However, the underlying mechanism remains largely unclear. Here, we observed that PFKFB3, a key glycolytic enzyme, was remarkably induced in kidney proximal tubular cells following ischemia-reperfusion injury in mice, as well as in multiple etiologies of chronic kidney disease patients. Proximal tubular epithelial-specific deletion of PFKFB3 significantly reduced renal lactate levels, mitigated inflammation and fibrosis, and preserved renal function in the IRI mouse model. To explore the mechanism of PFKFB3 in renal fibrosis, we performed RNA-sequencing (RNA-seq) on the kidney cortices from IRI mice. Of note, we found that PFKFB3-mediated kidney tubular glycolytic reprogramming markedly enhanced H4K12la lactylation. To further explore the potential functional significance of H4K12la in renal fibrosis, we performed genome-wide cleavage under targets and tagmentation (CUT&Tag) analysis to identify candidate genes regulated by H4K12la in sham and IRI kidney. Following CUT&Tag, H4K12la-associated DNAs were amplified using non-biased conditions, labeled, and sequenced with Illumina NovaSeq 6000.

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