Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Luminal Stem Cell Determinant SOX9 Controls Lineage Plasticity and Progression in Basal-Like Breast Cancer (ATAC-seq)

ABSTRACT: Luminal Stem Cell Determinant SOX9 Controls Lineage Plasticity and Progression in Basal-Like Breast Cancer (ATAC-seq)

PROVIDER: PRJNA576616 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10250792.fastq.gz	Fastqsanger.gz
	SRR10250793.fastq.gz	Fastqsanger.gz
	SRR10250794.fastq.gz	Fastqsanger.gz
	SRR10250795.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

Luminal Stem Cell Determinant SOX9 Controls Lineage Plasticity and Progression in Basal-Like Breast Cancer (Sox9-GFP)

Project description:Lineage plasticity plays an important role in the development of basal-like breast cancer (BLBC), an aggressive cancer subtype. Although studies suggest BLBC is likely to originate from luminal progenitor cells, it acquires substantial basal cell features and contains a heterogenous collection of cells exhibiting basal, luminal and bipotent phenotypes. Why luminal progenitors are prone to BLBC transformation and what drives luminal-to-basal/bipotent reprogramming remains unclear. Here we show that the transcription factor SOX9 acts as a determinant for ER– luminal stem/progenitor cells (LSPCs). SOX9 controls LSPC activity in part by activating both canonical and non-canonical NF-KB signaling. Inactivation of p53 and Rb in a BLBC mouse tumor model leads to upregulation of SOX9, which drives luminal-to-bipotent reprogramming in vivo. SOX9 deletion inhibits the progression of benign, neoplastic lesions to invasive carcinoma. Furthermore, SOX9 is overexpressed and correlated with shorter relapse-free survival in human BLBC. These data show that ER– LSPC determinant SOX9 acts as a lineage-specific driver for BLBC transformation.

2020-06-09 | GSE135885 | GEO

Luminal Stem Cell Determinant SOX9 Controls Lineage Plasticity and Progression in Basal-Like Breast Cancer (Sox9-KO)

Project description:Lineage plasticity plays an important role in the development of basal-like breast cancer (BLBC), an aggressive cancer subtype. Although studies suggest BLBC is likely to originate from luminal progenitor cells, it acquires substantial basal cell features and contains a heterogenous collection of cells exhibiting basal, luminal and bipotent phenotypes. Why luminal progenitors are prone to BLBC transformation and what drives luminal-to-basal/bipotent reprogramming remains unclear. Here we show that the transcription factor SOX9 acts as a determinant for ER– luminal stem/progenitor cells (LSPCs). SOX9 controls LSPC activity in part by activating both canonical and non-canonical NF-B signaling. Inactivation of p53 and Rb in a BLBC mouse tumor model leads to upregulation of SOX9, which drives luminal-to-bipotent reprogramming in vivo. SOX9 deletion inhibits the progression of benign, neoplastic lesions to invasive carcinoma. Furthermore, SOX9 is overexpressed and correlated with shorter relapse-free survival in human BLBC. These data show that ER– LSPC determinant SOX9 acts as a lineage-specific driver for BLBC transformation.

2020-06-09 | GSE135891 | GEO

Luminal Stem Cell Determinant SOX9 Controls Lineage Plasticity and Progression in Basal-Like Breast Cancer (ATAC-seq)

Project description:Lineage plasticity plays an important role in the development of basal-like breast cancer (BLBC), an aggressive cancer subtype. Although studies suggest BLBC is likely to originate from luminal progenitor cells, it acquires substantial basal cell features and contains a heterogenous collection of cells exhibiting basal, luminal and bipotent phenotypes. Why luminal progenitors are prone to BLBC transformation and what drives luminal-to-basal/bipotent reprogramming remains unclear. Here we show that the transcription factor SOX9 acts as a determinant for ER– luminal stem/progenitor cells (LSPCs). SOX9 controls LSPC activity in part by activating both canonical and non-canonical NF-B signaling. Inactivation of p53 and Rb in a BLBC mouse tumor model leads to upregulation of SOX9, which drives luminal-to-bipotent reprogramming in vivo. SOX9 deletion inhibits the progression of benign, neoplastic lesions to invasive carcinoma. Furthermore, SOX9 is overexpressed and correlated with shorter relapse-free survival in human BLBC. These data show that ER– LSPC determinant SOX9 acts as a lineage-specific driver for BLBC transformation.

2020-06-09 | GSE138631 | GEO

Luminal Stem Cell Determinant SOX9 Controls Lineage Plasticity and Progression in Basal-Like Breast Cancer (Sox9-GFP)

Project description:Luminal Stem Cell Determinant SOX9 Controls Lineage Plasticity and Progression in Basal-Like Breast Cancer (Sox9-GFP)

| PRJNA560404 | ENA

Luminal Stem Cell Determinant SOX9 Controls Lineage Plasticity and Progression in Basal-Like Breast Cancer (Sox9-KO)

Project description:Luminal Stem Cell Determinant SOX9 Controls Lineage Plasticity and Progression in Basal-Like Breast Cancer (Sox9-KO)

| PRJNA560490 | ENA

Luminal Stem Cell Determinant SOX9 Controls Lineage Plasticity and Progression in Basal-Like Breast Cancer

Project description:Luminal Stem Cell Determinant SOX9 Controls Lineage Plasticity and Progression in Basal-Like Breast Cancer

| PRJNA560487 | ENA

Lineage plasticity enables low-ER luminal tumors to evolve and gain basal-like traits

Project description:Breast tumors expressing lower levels of Estrogen Receptor (ER) represent a distinct subset of breast cancer characterized by the emergence of basal-like characteristics within tumors that are traditionally considered luminal-like. Lineage tracing of these low-ER tumors in the MMTV-PyMT mouse mammary tumor model revealed that the basal-like tumor cells within these tumors arose from normal luminal epithelial cells, suggesting that luminal-to-basal plasticity is responsible for the evolution and emergence of basal-like characteristics within these tumors. This study aims to identify the potential drivers of this plasticity by using single-cell RNA sequencing to identify populations of lineage-restricted luminal cells and luminal-derived basal cells within the tumor, and comparing their gene expression profiles.

2023-03-01 | GSE214815 | GEO

Inactivation of LATS1/2 drives luminal-basal plasticity to initiate basal-like mammary carcinomas

Project description:Basal breast cancers, an aggressive breast cancer subtype that has poor treatment options, are thought to arise from luminal mammary epithelial cells that undergo basal-like plasticity through poorly understood mechanisms. Using genetic mouse models and ex vivo primary organoid cultures, we show that conditional co-deletion of the LATS1 and LATS2 kinases, key effectors of Hippo pathway signaling, in mature mammary luminal epithelial cells promotes the development of basal-like carcinomas that metastasize over time. Genetic co-deletion experiments revealed that phenotypes resulting from the loss of LATS1/2 activity are dependent on the transcriptional regulators YAP/TAZ. Notably, transcriptional analyses of LATS1/2-deleted mammary epithelial cells revealed a gene expression program that associates with human basal breast cancers. Our study demonstrates in vivo roles for the LATS1/2 kinases in mammary epithelial homeostasis and luminal-basal fate control and implicates signaling networks induced upon the loss of LATS1/2 activity in the development of basal breast cancers.

2022-09-26 | GSE196555 | GEO

Inactivation of LATS1/2 drives luminal-basal plasticity to initiate basal-like mammary carcinomas

Project description:Inactivation of LATS1/2 drives luminal-basal plasticity to initiate basal-like mammary carcinomas

| PRJNA805501 | ENA

ONECUT2 is a druggable driver of luminal to basal breast cancer plasticity

Project description:ONECUT2 is a druggable driver of luminal to basal breast cancer plasticity

| PRJNA1013822 | ENA