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The H2BE76K mutation drives breast cancer development by enhancing the transcription of ADAM19

ABSTRACT: The H2BE76K mutation drives breast cancer development by enhancing the transcription of ADAM19

PROVIDER: PRJNA548915 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10611539_1.fastq.gz	Fastqsanger.gz
	SRR10611539_2.fastq.gz	Fastqsanger.gz
	SRR10611540_1.fastq.gz	Fastqsanger.gz
	SRR10611540_2.fastq.gz	Fastqsanger.gz
	SRR10611541_1.fastq.gz	Fastqsanger.gz

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The H2BE76K mutation drives breast cancer development by enhancing the transcription of ADAM19

Project description:Study was conducted to understand the effect of the cancer associated H2BE76K mutation. Using CRISPR/Cas9 Knock-in cell lines expressing FLAG-tagged WT and E76K mutant H2B, we conducted gene expression profiling experiments and studied the effect of the H2BE76K mutation on H2B occupancy using CUT&RUN sequencing.

2021-02-01 | GSE132749 | GEO

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TRIB3 Supports Breast Cancer Stemness by Suppressing FOXO1 Degradation and Enhancing SOX2 Transcription

Project description:The existence of breast cancer stem cells (BCSCs) is a major reason underlying cancer metastasis and recurrence after chemotherapy and radiotherapy. Targeting BCSCs may ameliorate breast cancer relapse and therapy resistance. Here, we report that expression of the pseudokinase Tribble 3 (TRIB3) positively associates with breast cancer stemness and progression. Elevated TRIB3 expression supports BCSCs by interacting with AKT to interfere with the FOXO1-AKT interaction and suppress FOXO1 phosphorylation, ubiquitination, and degradation by E3 ligases SKP2 and NEDD4L. The accumulated FOXO1 promotes transcriptional expression of SOX2, a transcriptional factor for cancer stemness, which in turn, activates FOXO1 transcription and forms a positive regulatory loop. Disturbing the TRIB3-AKT interaction suppresses BCSCs by accelerating FOXO1 degradation and reducing SOX2 expression in mouse models of breast cancer. Our study provides insights into breast cancer development and confers a potential therapeutic strategy against TRIB3-overexpressed breast cancer.

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Cancer-associated E239K mutation of LSD1 promotes the migration and invasion of luminal breast cancer cells by reducing the expression of ERα

Project description:Background: Epithelial to mesenchymal transition (EMT) plays an essential role in the metastasis of breast cancer by regulating the migration and invasion of cancer cells. Lysine specific demethylase 1 (LSD1) is an important histone demethylase that mediates EMT. However, the functional effects of the mutation on LSD1 in breast cancer remain unclear. Results: An E239K mutation of LSD1 was identified from TCGA Breast Invasive Carcinoma cohort. To investigate the functional effects of the E239K mutation of LSD1, a stable LSD1 knockdown MCF7 cell line was generated. Rescue with the wild-type LSD1, but not the E239K mutated LSD1, suppressed the increased invasion of the LSD1 knockdown cells, demonstrating that the E239K mutation abolished the suppressive effects of LSD1 on the invasion of breast cancer cells. Further analysis showed that the E239K mutation of LSD1 led to decreased expression of estrogen receptor α (ERα), which subsequently increased the expression of Slug, a master transcription factor that promoted EMT. Most importantly, the E239K mutation of LSD1 disrupted the interaction between LSD1 and GATA3, which reduced the enrichment of LSD1 at the promoter region of ERα gene. The reduced enrichment of LSD1 at the promoter region of ERα gene caused enhanced histone H3K9 methylation, which in turn suppressed the transcription of ERα gene. Conclusions: The E239K mutation of LSD1 promotes the migration and invasion of breast cancer cells by disrupting the interaction between LSD1 and GATA3, which reduces the expression of ERα by enhancing the histone H3K9 methylation.

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