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Unravelling subclonal heterogeneity and aggressive disease states in TNBC through single-cell RNA-seq [RNA-Seq]

ABSTRACT: Unravelling subclonal heterogeneity and aggressive disease states in TNBC through single-cell RNA-seq [RNA-Seq]

PROVIDER: PRJNA485429 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7666350_1.fastq.gz	Fastqsanger.gz
	SRR7666350_2.fastq.gz	Fastqsanger.gz
	SRR7666360_1.fastq.gz	Fastqsanger.gz
	SRR7666360_2.fastq.gz	Fastqsanger.gz
	SRR7666370_1.fastq.gz	Fastqsanger.gz

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Unravelling subclonal heterogeneity and aggressive disease states in TNBC through single-cell RNA-seq

Project description:Unravelling subclonal heterogeneity and aggressive disease states in TNBC through single-cell RNA-seq

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Unravelling subclonal heterogeneity and aggressive disease states in TNBC through single-cell RNA-seq [WES]

Project description:Unravelling subclonal heterogeneity and aggressive disease states in TNBC through single-cell RNA-seq [WES]

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Unravelling subclonal heterogeneity and aggressive disease states in TNBC through single-cell RNA-seq [RNA-Seq]

Project description:Triple-negative breast cancer (TNBC) is an aggressive subtype characterized by extensive intratumoral heterogeneity. To investigate the underlying biology, we conduct single-cell RNA- sequencing (scRNA-seq) of >1500 cells from six primary TNBC. Intercellular heterogeneity of gene expression programs within each tumor was variable and largely correlated with clonality of inferred genomic copy number changes, suggesting that genotype drives the gene expression phenotype of individual subpopulations. Clustering of gene expression profiles identified distinct subgroups of malignant cells shared by multiple tumors, including a single subpopulation associated with multiple signatures of treatment resistance and metastasis, and characterized functionally by activation of glycosphingolipid metabolism and associated innate immunity pathways. A novel signature defining this subpopulation was predictive of long-term outcomes for TNBC patients in a large patient cohort. Collectively, this analysis reveals the functional heterogeneity and its association with genomic evolution in TNBC, and uncovers unanticipated biological principles dictating poor outcomes in this disease.

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Unravelling subclonal heterogeneity and aggressive disease states in TNBC through single-cell RNA-seq [WES]

Project description:Triple-negative breast cancer (TNBC) is an aggressive subtype characterized by extensive intratumoral heterogeneity. To investigate the underlying biology, we conduct single-cell RNA- sequencing (scRNA-seq) of >1500 cells from six primary TNBC, together with whole exome sequencing (WES) for four of the tumors. Intercellular heterogeneity of gene expression programs within each tumor was variable and largely correlated with clonality of inferred genomic copy number changes, suggesting that genotype drives the gene expression phenotype of individual subpopulations. Clustering of gene expression profiles identified distinct subgroups of malignant cells shared by multiple tumors, including a single subpopulation associated with multiple signatures of treatment resistance and metastasis, and characterized functionally by activation of glycosphingolipid metabolism and associated innate immunity pathways. A novel signature defining this subpopulation was predictive of long-term outcomes for TNBC patients in a large patient cohort. Collectively, this analysis reveals the functional heterogeneity and its association with genomic evolution in TNBC, and uncovers unanticipated biological principles dictating poor outcomes in this disease.

2018-08-11 | GSE118303 | GEO

Unravelling subclonal heterogeneity and aggressive disease states in TNBC through single-cell RNA-seq.

Project description:Triple-negative breast cancer (TNBC) is an aggressive subtype characterized by extensive intratumoral heterogeneity. To investigate the underlying biology, we conducted single-cell RNA-sequencing (scRNA-seq) of >1500 cells from six primary TNBC. Here, we show that intercellular heterogeneity of gene expression programs within each tumor is variable and largely correlates with clonality of inferred genomic copy number changes, suggesting that genotype drives the gene expression phenotype of individual subpopulations. Clustering of gene expression profiles identified distinct subgroups of malignant cells shared by multiple tumors, including a single subpopulation associated with multiple signatures of treatment resistance and metastasis, and characterized functionally by activation of glycosphingolipid metabolism and associated innate immunity pathways. A novel signature defining this subpopulation predicts long-term outcomes for TNBC patients in a large cohort. Collectively, this analysis reveals the functional heterogeneity and its association with genomic evolution in TNBC, and uncovers unanticipated biological principles dictating poor outcomes in this disease.

| S-EPMC6123496 | biostudies-literature

Unravelling subclonal heterogeneity and aggressive disease states in TNBC through single-cell RNA-seq

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-08-11 | GSE118390 | GEO

Transcriptome profiling of tumors from Kenyan triple negative breast cancer (TNBC) patients.

Project description:Triple negative breast cancer is an aggressive phenotypic breast cancer characterized by ER negative, PR negative and Her2 negative immunohistochemistry status. We embarked on a study to explore the transcriptome of Kenyan TNBC patients and identify potential biomarkers specific to Kenyan population. The transcriptome sequencing of tumors from Kenyan TNBC patients and comparisons with African American and Caucasian TNBC transcriptomes revealed several interesting targets and dysregulated pathways.

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Project description:The pattern recognition receptor long pentraxin-3 (PTX3) plays conflicting roles in cancer by acting as an oncosuppressor or as a pro-tumor mediator depending on tumor context. Triple negative breast cancer (TNBC) represents the most aggressive histotype of breast cancer, characterized by the lack of efficacious therapeutic targets/approaches and poor prognosis. In this study, in silico data and experimental evidences indicate that PTX3 is produced by tumor parenchyma in TNBC and that its expression levels correlate with tumor stage. On this basis, the impact of PTX3 silencing or its overexpression on the tumorigenic potential of TNBC cell lines was analyzed. Gene expression and in vitro results demonstrate that high levels of PTX3 expression confer a high aggressive/proliferative phenotype, fosters stem-like features, and rewires the energy metabolism in TNBC cells. This results in a more tumorigenic potential in vivo when TNBC cells are grafted in immune-compromised and syngeneic animals. Mechanistically, our data reveal a strong positive correlation between PTX3 expression and the antitumor activity of Toll-like receptor 4 (TLR4) inhibition in TBNC, demonstrating for the first time that PTX3-driven TNBC aggressiveness is due to PTX3-mediated activation of TLR4 signaling. Altogether, these data shed light on the role of tumor-produced PTX3 in TNBC and uncover the importance of the PTX3/TLR4 pathway for therapeutic and prognostic exploitation in TNBC.

2021-11-06 | GSE188315 | GEO

Transcriptomes of triple-negative breast cancer (TNBC) cells (SUM159) and non-TNBC cells (HCC1569) that overexpressed JMJD6 were compared

Project description:The expression levels of JMJD6 and its correlation with H2A.XY39ph differed in TNBC and non-TNBC cells. In addition, we have previously shown that H2A.XY39ph levels are positively correlated with tumor size, histological grade and advanced TNM stage in breast cancer. To analyze the role of JMJD6 in regulating the characteristics of different subtypes of breast cancer, the transcriptomes of TNBC cells (SUM159) and non-TNBC cells (HCC1569) that overexpressed JMJD6 were compared. We speculate that JMJD6 overexpression cause autophagy pathway activation in TNBC via enhancing ATG genes expression.

2023-10-01 | E-MTAB-6517 | biostudies-arrayexpress

CDK5 inhibition abrogates TNBC stem-cell property and enhances anti-PD-1 therapy

Project description:Triple-negative breast cancer (TNBC) is a highly aggressive subtype of breast cancer that shows high infiltration of cancer stem cells (CSCs), which correlates with poor clinical outcome. Here, we have demonstrated that an aberrant activation of CDK5/pho-PPARg axis associated with TNBC progression closely. CDK5 blockade sufficiently abrogates stemness transformation of TNBC cells, resulting in a significant inhibition of tumor metastatic progression. Moreover, CDK5 inhibitor Rosc attenuates CD44v+ BCSCs, hereby reversing immunosuppressive microenvironment and enhancing anti-PD-1 effects on TNBC. Mechanistically, CDK5/pho-PPARgaxis modulates the ESRP1 degradation via E3 ligase-like activity, leading to CD44 variant (CD44v) expression. Our finding indicates that CDK5 blockade could be a potent strategy to target CSCs in TNBC, and to increase the response to PD-1 blockade in TNBC therapy.

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