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Inhibition of TNBC metastasis by Gpx1

ABSTRACT: Inhibition of TNBC metastasis by Gpx1

PROVIDER: PRJNA522914 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8586200_1.fastq.gz	Fastqsanger.gz
	SRR8586200_2.fastq.gz	Fastqsanger.gz
	SRR8586201_1.fastq.gz	Fastqsanger.gz
	SRR8586201_2.fastq.gz	Fastqsanger.gz
	SRR8586202_1.fastq.gz	Fastqsanger.gz

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Inhibition of TNBC metastasis by Gpx1

Project description:Gpx1 plays a vital role in the metastasis of TNBC cells by regulating cell adhesion. Depletion of Gpx1 reduces the survival, migration, and invasion of TNBC cells in vitro. Transcriptomic and signaling pathway analyses demonstrate that depletion of Gpx1 essentially impairs cell adhesion/spreading by down-regulating FAK/c-Src activation.

2019-11-30 | GSE126675 | GEO

EZH2-H3K27me3 mediated KRT14 upregulation promotes TNBC peritoneal metastasis

Project description:Triple-Negative Breast Cancer (TNBC) has a poor prognosis and adverse clinical outcomes among all breast cancer subtypes as there is no available targeted therapy. Overexpression of Enhancer of zeste homolog 2 (EZH2) has been shown to correlate with TNBC's poor prognosis, but the contribution of EZH2 catalytic (H3K27me3) versus non-catalytic EZH2 (NC-EZH2) function in TNBC progression remains elusive. We reveal that selective hyper-activation of functional EZH2 (H3K27me3) over NC-EZH2 alters TNBC metastatic landscape and fosters its peritoneal metastasis, particularly splenic. Instead of H3K27me3-mediated repression of gene expression; here, it promotes KRT14 transcription by attenuating binding of repressor Sp1 to its promoter. Further, KRT14 loss significantly reduces TNBC migration, invasion, and peritoneal metastasis. Consistently, human TNBC metastasis displays positive correlation between H3K27me3 and KRT14 levels. Finally, EZH2 knockdown or H3K27me3 inhibition by EPZ6438 reduces TNBC peritoneal metastasis. Altogether, our preclinical findings suggest a rationale for targeting TNBC with EZH2 inhibitors.

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Verteporfin targets CCR5 to inhibit TNBC growth and metastasis via YAP1

Project description:CCL5/CCR5 axis is an immunotherapeutic target for triple-negative breast cancer (TNBC). However, the signaling mechanism is poorly understood and its antagonists have not been reported. Here, we developed a high-throughput screening (HTS) assay for discovering its antagonists. Verteporfin was identified as a specific and more potent inhibitor than maraviroc. It significantly reduced TNBC tumor growth in an immunologically dependent manner, and lung metastasis in a cell-intrinsic way. Mechanistically, CCR5 was co-expressed with Yes-associated protein 1 (YAP1) in TNBC patients. RNA-sequencing and expression silencing further revealed that CCR5 promoted the expression of YAP1 through HIF-1α in TNBC cells, and through YAP1 to regulate β-catenin, ZEB1/ZEB2 for metastasis, as well as CXCL16 and CXCL8 for immune cell migration and tumor growth. In essence, verteporfin may have potential immunotherapeutic applications for diseases co-expressing CCR5 and YAP1 such as TNBC. The HTS assay can be adapted for unveiling antagonists of broader signaling pathways.

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EZH2-H3K27me3 mediated KRT14 upregulation promotes TNBC peritoneal metastasis

Project description:EZH2-H3K27me3 mediated KRT14 upregulation promotes TNBC peritoneal metastasis

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POGZ loss increases TGFβ signaling and potentiates TNBC metastasis

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POGZ loss increases TGFβ signaling and potentiates TNBC metastasis

Project description:The pogo transposable element derived zinc finger protein, POGZ, is notably associated with autism-like or intellectual disabilities through its role in gene transcription. Indeed, many proteins involved in neurological development are often dysregulated in cancer. We provide the first experimental evidence that POGZ influences the growth and metastatic spread of triple negative breast cancers (TNBC). Utilizing a well-characterized immunocompetent model of TNBC, we show that POGZ exerts a dual role, both as a tumor promoter and metastasis suppressor. Mechanistically, we show that POGZ loss potentiates TGFβ pathway activation in TNBC, to exert cytostatic effects while simultaneously increasing the mesenchymal and migratory properties of breast tumors. Finally, we demonstrate that whereas POGZ levels are elevated in human breast cancers, the most aggressive TNBC tumors, including those with increased mesenchymal and metastatic properties, dampen POGZ levels, associated with inferior clinical outcomes. Combined these data suggest that POGZ is a critical regulator of the early stages of metastatic cascade

2024-07-31 | GSE247628 | GEO

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Project description:N-acylsphingosine amidohydrolase (ASAH1) expression is elevated in many cancer types including breast cancer. Therefore, we analyzed the role of ASAH1 in TNBC. Inhibition of ASAH1 expression in TNBC cell lines resulted in decreased tumor growth and metastasis

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2024-09-03 | GSE264627 | GEO

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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