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Host CLIC4 is essential for breast cancer metastatic competence

ABSTRACT: Host CLIC4 is essential for breast cancer metastatic competence

PROVIDER: PRJNA767846 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16151313_1.fastq.gz	Fastqsanger.gz
	SRR16151313_2.fastq.gz	Fastqsanger.gz
	SRR16151314_1.fastq.gz	Fastqsanger.gz
	SRR16151314_2.fastq.gz	Fastqsanger.gz
	SRR16151315_1.fastq.gz	Fastqsanger.gz

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Host CLIC4 is essential for breast cancer metastatic competence

Project description:Chloride Intracellular Channel 4 (CLIC4) expression is elevated in the stroma of many cancers. We show that CLIC4 expression is higher in breast cancers from younger women and early stage metastatic disease, portends poor prognosis, and is linked to TGF-β expression. Two murine breast cancer models with lung metastases revealed that ablation of host Clic4 nearly eliminated lung metastases without reducing primary tumor size while Clic4 null tumor cells retained metastatic capability. Thus, CLIC4 is required for host metastatic competence. Deficiencies in circulating pro-metastatic soluble factors were detected in CLIC4 deficient hosts bearing primary tumors. Necrosis and vascular abnormalities were more abundant in primary tumors from CLIC4 deficient hosts than from CLIC4 proficient control hosts. Transcriptional profiles of lungs and primary tumors prior to the onset of metastases indicated that loss of host CLIC4 enhances an inflammatory microenvironment. Thus, CLIC4 expression in human breast cancers may serve as a prognostic biomarker, and targeting host CLIC4 could reduce metastatic competence.

2022-05-25 | GSE185163 | GEO

Host CLIC4 is essential for breast cancer metastatic competence

Project description:Host CLIC4 is essential for breast cancer metastatic competence

| PRJNA767846 | ENA

CLIC4 is essential for host competence for metastasis in murine models of breast cancer and a prognostic indicator for human breast cancer

Project description:CLIC4 belongs to a family of highly conserved metamorphic proteins of the glutathione‐S‐transferase superfamily and dysregulation is implicated in pulmonary arterial hypertension, asthma, and ovarian cancer. We show that genetic ablation of host Clic4 eliminated the establishment of breast cancer lung metastases in two independent mouse models while Clic4 null tumor cells retained metastatic capability. TCGA and METABRIC data indicated that CLIC4 is elevated in human breast cancers from young women, those with poor prognosis and those with early stage metastatic disease. Experimentally, the essential Clic4 host contributions for metastatic competence depended on circulating levels of pro‐ metastatic mediators, neoangiogenesis, tumor cell attachment to lung tissue, myofibroblast differentiation, and leukocyte migration. CLIC4 was abundant in circulating extracellular vesicles (EVs) from tumor‐bearing wildtype mice but absent in EVs from tumor‐bearing Clic4 null hosts or wildtype hosts bearing Clic4 null‐tumors suggesting cross‐talk between host and tumor cells is required to deposit CLIC4 in EVs. These results illuminate CLIC4 as a critical host factor for metastatic competence, a potential prognostic marker for breast cancer patients and a target for anti‐metastatic therapy.

2020-11-26 | GSE141057 | GEO

CLIC4 is essential for host competence for metastasis in murine models of breast cancer and a prognostic indicator for human breast cancer

Project description:CLIC4 is essential for host competence for metastasis in murine models of breast cancer and a prognostic indicator for human breast cancer

| PRJNA591906 | ENA

Host CLIC4 expression in the tumor microenvironment is essential for breast cancer metastatic competence.

Project description:The TGF-β-regulated Chloride Intracellular Channel 4 (CLIC4) is an essential participant in the formation of breast cancer stroma. Here, we used data available from the TCGA and METABRIC datasets to show that CLIC4 expression was higher in breast cancers from younger women and those with early-stage metastatic disease. Elevated CLIC4 predicted poor outcome in breast cancer patients and was linked to the TGF-β pathway. However, these associations did not reveal the underlying biological contribution of CLIC4 to breast cancer progression. Constitutive ablation of host Clic4 in two murine metastatic breast cancer models nearly eliminated lung metastases without reducing primary tumor weight, while tumor cells ablated of Clic4 retained metastatic capability in wildtype hosts. Thus, CLIC4 was required for host metastatic competence. Pre- and post-metastatic proteomic analysis identified circulating pro-metastatic soluble factors that differed in tumor-bearing CLIC4-deficient and wildtype hosts. Vascular abnormalities and necrosis increased in primary tumors from CLIC4-deficient hosts. Transcriptional profiles of both primary tumors and pre-metastatic lungs of tumor-bearing CLIC4-deficient hosts were consistent with a microenvironment where inflammatory pathways were elevated. Altogether, CLIC4 expression in human breast cancers may serve as a prognostic biomarker; therapeutic targeting of CLIC4 could reduce primary tumor viability and host metastatic competence.

| S-EPMC9249210 | biostudies-literature

A model that cancer cells’ metastatic competence is determined by their states

Project description:A polyclonal mouse model of breast tumor heterogeneity using model cell line 4T1 was developed previously. It was shown that 4T1 cells were composed of mixed subpopulations with specializations, including dominating the primary tumor, contributing to metastatic populations, etc. Here in a different angle, we reveal that each 4T1 cells can switch between 2 distinct states, which could be easily misclassified into 2 subpopulations, as the 2 states can be distinguished by distinct patterns of gene expression, dramatic difference of metastatic competence, stem-cell like feature or not, etc. The event for each 4T1 cell to exhibit one state or another is stochastic and the metastatic competence of clones generated from a single 4T1 cell is variable rather than stable. Further, given that metastatic competence of 4T1 cells is not stable, classification of clones based on metastatic competence is highly biased. Similarly, the classification of 4T1 clones based on gene expression profiles is also highly biased. Taken together, our data support that the exhibition of metastatic competence depends on the state of 4T1 cells and do not support the existence of subpopulations with specialization. To the best of our knowledge, no similar work has ever been reported.

2018-03-20 | GSE112038 | GEO

Proteomics of CLIC4 overexpressing human pulmonary artery endothelial cells

Project description:To identify CLIC4 effectors by studying proteins expressiosn altered by CLIC4 overexpression in human pulmonary artery endothelial cells.

2018-10-16 | PXD008714 | Pride

CLIC4 interacting proteins - To identify proteins in human pulmonary artery endothelial cells that interact with CLIC4

Project description:To identify proteins in human pulmonary artery endothelial cells that interact with CLIC4

2018-10-16 | PXD008709 | Pride

CLIC4 deficiency alters mitochondrial function and transcriptional profiles in murine breast cancer cells.

Project description:We report the different transcriptom of 6DT1 (murine mammary cancer cell line) wildtype cells or CLIC4-KO (by CRISPR cas9) untreated or treated 1uM H2O2 for 24 hours.

2022-09-14 | GSE173997 | GEO

Retinal pigment epithelium-specific CLIC4 mutant is a mouse model of dry age-related macular degeneration

Project description:Purpose: Bulk RNA-seq was perform to profile changes in 3-month-old mouse RPE cells caused by CLIC4 deficinecy

2021-12-21 | GSE191077 | GEO