Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The role of DOT1L in ovarian cancer growth and progression

ABSTRACT: The role of DOT1L in ovarian cancer growth and progression

PROVIDER: PRJNA663771 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12650367.fastq.gz	Fastqsanger.gz
	SRR12650368.fastq.gz	Fastqsanger.gz
	SRR12650369.fastq.gz	Fastqsanger.gz
	SRR12650370.fastq.gz	Fastqsanger.gz
	SRR12650371.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

The role of DOT1L in ovarian cancer growth and progression

Project description:Disruptor of telomeric silencing 1-like (DOT1L) expression is elevated in many cancer types including ovarian cancer. Therefore, we analyzed the role of DOT1L in ovarian cancer. Pharmacological inhibition of DOT1L expression in ovarian cancer cell lines resulted in decreased proliferation, and increased cell death.

2023-09-15 | GSE158019 | GEO

The role of ATAD2 in ovarian cancer growth and progression

Project description:The role of ATAD2 in ovarian cancer growth and progression

| PRJNA792585 | ENA

Functional effect of DOT1L pharmacological inhibition in ERα-positive Ovarian Cancer cells

Project description:Estrogen Receptor alpha (ERα), a nuclear receptor with transcriptional activity, is a master regulator of estrogen signaling, widely known as therapeutic target in hormone-responsive breast cancer (BC). Moreover, ERα is highly expressed in approximately 80% of High Grade Serous Ovarian Cancer (HGSOC), the most common epithelial ovarian carcinoma. Despite some promising clinical trials evaluating endocrine therapy in this type of tumor, the role of ERα is still unknown. Epigenetic changes, such as DNA methylation, are emerging as key contributing factors to carcinogenesis. Disruptor of telomeric silencing-1-like (DOT1L), the only known histone methyl transferase capable to produce H3K79 mono, di and tri-methylation, modulates ERα actions in hormone-responsive BC. Considering this evidence, ERα-DOT1L association was confirmed in ERα-positive OC cells, PEO1 and PEO4, by Co-IP. DOT1L pharmacological inhibition by EPZ004777 (EPZ) revealed the involvement of this epigenetic enzyme in cell proliferation, cell cycle progression and apoptosis. Transcriptome profiling after ICI (a Selective Estrogen Receptor Degrader) and EPZ treatment, in both cell lines, has underlined a deep impact of both compounds on ERα-modulated genes, including the down-regulation of ERα itself. On the other hand, functional analysis showed that commonly affected transcripts are involved in different cellular processes, such as cancer cell survival, chemoresistance and cell cycle progression. Moreover, ChIP-qPCR performed on ERα promoter highlighted ERα and DOT1L co-localization, both in PEO1 and in PEO4 cells, which was reduced after EPZ treatment, suggesting a role of this complex on receptor transcriptional activity. In addition, drug combination studies performed with EPZ and ICI showed an additive effect in cell growth inhibition. Taken together, these results suggest DOT1L as a potential therapeutic target in the treatment of OC.

2019-11-04 | E-MTAB-8198 | biostudies-arrayexpress

The role of ATAD2 in ovarian cancer growth and progression

Project description:ATPase Family AAA domain containing 2 (ATAD2) expression is elevated in many cancer types including ovarian cancer. Therefore, we analyzed the role of ATAD2 in ovarian cancer. Pharmacological inhibition of ATAD2 expression in ovarian cancer cell lines resulted in decreased proliferation, and increased cell death.

2024-12-01 | GSE192673 | GEO

The role of UBE2T in breast cancer growth and progression

Project description:The role of UBE2T in breast cancer growth and progression

| PRJNA658487 | ENA

The role of CDC7 in Melanoma cancer growth and progression

Project description:The role of CDC7 in Melanoma cancer growth and progression

| PRJNA665990 | ENA

The role of DOT1L in Th cells

Project description:The role of DOT1L in Th cells

| PRJNA577453 | ENA

DOT1L regulates pericentromeric heterochromatin

Project description:Many repetitive DNA elements are packaged in heterochromatin, but depend on occasional transcription to maintain long-term silencing. The factors that promote transcription of repeat elements in heterochromatin are largely unknown. Here, we show that DOT1L, a histone methyltransferase that modifies lysine 79 of histone H3 (H3K79), is required for transcription of major satellite repeats to maintain pericentromeric heterochromatin (PCH), and that this function is essential for preimplantation development. DOT1L is a transcriptional activator at single-copy genes but does not have a known role in repeat element transcription. We show that H3K79me3 is specifically enriched at repetitive elements, that loss of DOT1L compromises pericentromeric major satellite transcription, and that this function depends on interaction between DOT1L and the chromatin remodeler SMARCA5. DOT1L inhibition causes chromosome breaks and cell cycle defects, and leads to embryonic lethality. Together, our findings uncover a vital new role for DOT1L in transcriptional activation of heterochromatic repeats.

2023-05-26 | PXD028824 | Pride

DOT1L protects neural stem cells from ER stress

Project description:In order to understand the role of H3K79me2 and DOT1L during CNS development, we analysed neural stem cells after pharmacological inhibition of DOT1L (5 µM SGC0946). To identify target genes of DOT1L in the cortex, we determined the transcriptome of cortical progenitor cells derived from E14.5 NMRI mice after interference with DOT1L activity for three days in vitro (DIV3). Therefore, three independent experiments were performed (ctrl1 – inh1, ctrl2 – inh2, ctrl3 – inh3).

2015-12-31 | E-MTAB-3521 | biostudies-arrayexpress

The role of ASAH1 in Triple negative breast cancer (TNBC) growth and progression

Project description:The role of ASAH1 in Triple negative breast cancer (TNBC) growth and progression

| PRJNA1040259 | ENA