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Effect of inhibition of Setdb1 on gene expression in AML12 cells

ABSTRACT: Effect of inhibition of Setdb1 on gene expression in AML12 cells

PROVIDER: PRJNA937224 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23573633.fastq.gz	Fastqsanger.gz
	SRR23573634.fastq.gz	Fastqsanger.gz
	SRR23573635.fastq.gz	Fastqsanger.gz
	SRR23573636.fastq.gz	Fastqsanger.gz
	SRR23573637.fastq.gz	Fastqsanger.gz

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Effect of inhibition of Setdb1 on gene expression in AML12 cells

Project description:To investigate the mRNA expression regulated by Setdb1, we established AML12 knockdown cell model by infecting Setdb1 siRNA for 72 hours

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Project description:DUSP6 plays important roles in MAPK signaling pathway, but whether and how it is involved in liver funciton remains to be explored. Here, we performed RNA-seq analyses in AML12 cells where DUSP6 is disrupted. We overexpressed GFP-DUSP6 or GFP in AML12 cells, and tested the effects of DUSP6 increase on gene expression in AML12 cells. Meanwhile, we knocked down DUSP6 in AML12 cells and tested the effects of DUSP6 decrease on gene expression in AML12 cells. Taken together, we analyzed the changes of gene expression mediated by DUSP6, which provides new insights for the function of DUSP6 in liver

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Effect of prolactin and actinomycin D on gene expression in murine AML12 and Hepa 1-6 hepatocytes

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Expression (Gene) array from AMl12-Zfp125- stably expressing cells

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Cytoplasmic localization of SETDB1 induced Warburg effect via c-MYC/ LDHA axis to enhance migration and invasion in breast carcinoma

Project description:SETDB1, a pivotal histone lysine methyltransferase, has been identified as being transported to the cytoplasm through a CMR1-dependent pathway, contributing to non-histone methylation. However, the function and underlying mechanism of cytoplasmic SETDB1 in breast cancer remain elusive. This study, employing immunohistochemistry, revealed that an elevated level of cytoplasmic SETDB1 is correlated with lymph node metastasis and more aggressive breast cancer subtypes. Functionally, cytoplasmic SETDB1 proves indispensable for cell migration and invasion, as well as the induction of epithelial-mesenchymal transition (EMT), which could be reversed by LMB (a CMR1 inhibitor) treatment. Furthermore, it was observed that cytoplasmic SETDB1 elevates the levels of metabolites associated with the Warburg effect, including glucose, pyruvate, lactate, and ATP. Mechanistically, the release of nuclear SETDB1 alleviates the inhibition of c-MYC transcription, leading to increased c-MYC expression and subsequent up-regulation of LDHA expression. Notably, LDHA overexpression enhanced migration and invasion by inducing EMT, while its depletion can reverse SETDB1-induced migration and invasion, as well as the Warburg effect and EMT. In conclusion, the subcellular localization of cytoplasmic SETDB1 emerges as a pivotal factor in breast cancer progression. This study offers valuable insights into the novel functions and mechanisms of cytoplasmic SETDB1.

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