Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Polo-like kinase 1 inhibitors differentiate triple-negative breast cancer towards a luminal cell fate

ABSTRACT: Polo-like kinase 1 inhibitors differentiate triple-negative breast cancer towards a luminal cell fate

PROVIDER: PRJNA763910 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR15915300_1.fastq.gz	Fastqsanger.gz
	SRR15915300_2.fastq.gz	Fastqsanger.gz
	SRR15915301_1.fastq.gz	Fastqsanger.gz
	SRR15915301_2.fastq.gz	Fastqsanger.gz
	SRR15915302_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 96

Similar Datasets

Polo-like kinase 1 inhibitors differentiate triple-negative breast cancer towards a luminal cell fate

Project description:Transcriptomic profiling was applied to investigate the effects of polo-like kinase 1 inhibition in triple-negative breast cancer.

2022-08-29 | GSE184295 | GEO

Polo-like kinase 1 inhibitors differentiate triple-negative breast cancer towards a luminal cell fate

Project description:Plasticity delineates cancer subtypes with more or less favourable outcomes. In breast cancer, triple-negative is the subtype that lacks the expression of major differentiation markers (i.e. estrogen receptor [ER]), ant its high cellular plasticity results in higher aggressiveness and poor prognosis compared to other subtypes. Whether plasticity poses a vulnerability to cancer cells remains elusive. Here, we show that cancer cell plasticity can be exploited to differentiate triple-negative breast cancer. Using a high-throughput reporter drug screen with 9,501 compounds, we identify three polo-like kinase 1 (PLK1) inhibitors as major inducers of ER protein expression and downstream activity in triple-negative breast cancer cells via the transcription factor BATF. PLK1 inhibition upregulates a cell differentiation program characterized by increased DNA damage, mitotic arrest and ultimately cell death. Notably, cells surviving PLK1 inhibition have decreased tumorigenic potential, and targeting PLK1 in already established tumours reduces tumour growth both in cell line and patient-derived xenograft models. In addition, genes upregulated upon PLK1 inhibition are correlated with expression in normal breast tissue and confer better overall survival in breast cancer patients. Our results indicate that differentiation therapy based on PLK1 inhibition might be an alternative strategy to treat triple-negative breast cancer.

2022-08-23 | PXD028495 | Pride

Alveolar basal cells differentiate towards secretory epithelial and aberrant basaloid cells in vitro

Project description:Alveolar basal cells differentiate towards secretory epithelial and aberrant basaloid cells in vitro

| PRJNA813874 | ENA

Bulk mitotic ATACseq for Polo-like kinase 1 maintains transcription and chromosomal accessibility during mitosis

Project description:We found that Polo-like kinase 1 (Plk1) activity directly on chromatin sustains global transcription and chromosomal accessibility in mitosis. Inhibition of Plk1 leads to significant overall downregulation of accessibility on mitotic chromosomes, especially at promoter and transcription start site (TSS) regions. Therefore, Plk1 activity sustains global chromosomal accessibility in mitosis, facilitating transcription factor binding and ensuring proper transcriptional activity, which maintains mitotic fidelity.

2025-11-18 | GSE282486 | GEO

Pparg drives luminal differentiation and luminal tumor formation in the urothelium

Project description:We find that Pparg is a master regulator of cell specification during urothelial homeostasis, driving a luminal differentiation program via retinoid signaling. Interestingly, expression of activated Pparg in basal cells only drives tumor formation when they are in an activated state, that are in an activated state, induces formation of luminal tumors with papillary morphology, Expression of an activated form of Pparg induces basal cells at homeostasis, to differentiate directly into luminal cells. In a BBN mouse model which produces basal subtypes tumors in wild type animals, activated Pparg drives formation of luminal tumors, suggesting that this transcription factor is a master regulator of luminal differentiation, as has been suggested from in vitro studies.

2021-09-22 | GSE172656 | GEO

Bulk RNA-seq of a time series of hPSCs as they differentiate towards left ventricle cardiomyocytes

Project description:Bulk RNA-seq of a time series of hPSCs as they differentiate towards left ventricle cardiomyocytes

| PRJNA839709 | ENA

Two Forkhead transcription factors regulate cardiac progenitor cell divisions by a Polo kinase-dependent pathway

Project description:The development of a complex organ requires the proper differentiation and production of appropriate numbers of each of its constituent cell types, as well as their correct positioning within the organ. During Drosophila cardiogenesis, all three of these processes are controlled by jumeau (jumu) and Checkpoint suppressor homologue (CHES-1-like), two genes encoding forkhead transcription factors that were discovered utilizing an integrated genetic, genomic and computational strategy which identified 70 novel genes expressed in the developing Drosophila heart. Both jumu and CHES-1-like are required during asymmetric cell division for the derivation of two distinct cardiac cell types from their mutual precursor, and in symmetric cell division to produce yet a third type of heart cell. jumu and CHES-1-like control the division of cardiac progenitors by regulating the activity of Polo, a kinase involved in multiple steps of mitosis. This pathway demonstrates how transcription factors integrate diverse developmental processes during organogenesis. GFP-positive cells were profiled from Stage 11-12 Drosophila embryos of the following two genotypes: twi-GAL4 UAS-2EGFP/UAS-jumu and twi-GAL4 UAS-2EGFP

2012-01-30 | E-GEOD-34946 | biostudies-arrayexpress

Polo-like kinase inhibitors increase AAV production by halting cell cycle progression

Project description:Polo-like kinase inhibitors increase AAV production by halting cell cycle progression

| PRJNA1142858 | ENA

Polo-like kinase inhibitors increase AAV production by halting cell cycle progression

Project description:Recombinant Adeno-associated viruses (rAAV) are commonly used in gene therapy for preclinical research and therapeutic applications. Despite its clinical efficacy, the manufacturing of rAAV faces challenges in productivity and quality, leading to limited availability. In this study, we aimed to identify compounds that increase the capacity of cells to produce AAV9 with a high-throughput small-molecule screening strategy. With the Arrayed Targeted Library for AAV Screening platform, we screened a library of 3,300 small molecules and identified several targets, including cell-cycle modulators, G protein-coupled receptor modulators, histone deacetylate inhibitors, Janus kinase inhibitors, and metabolic modulators. Most notably, we identified Polo-like kinase isoform 1 (PLK1) inhibitors as enhancers of AAV production. PLK1 inhibition using HMN-214 increased AAV production, and was largely consistent across HEK293 cell lines, vector payloads and capsid serotypes. Using cell cycle and RNA-sequencing analysis, we show that PLK1 inhibition halts cells in the G2/M phase and blocks their exit from the M to G1 phase. These findings can be used to develop more cost-effective methods to increase AAV yield during production in the manufacturing process.

2025-01-22 | GSE273692 | GEO

Endovascular progenitors invade melanoma tumors and differentiate towards a variety of vascular beds to promote tumor metastasis

Project description:Endovascular progenitors invade melanoma tumors and differentiate towards a variety of vascular beds to promote tumor metastasis

| PRJNA471691 | ENA

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data