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The oxidoreductase CLIC4 is required to maintain mitochondrial function and resistance to exogenous oxidants in breast cancer cells.

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE188780 | GEO | 2022/07/15

REPOSITORIES: GEO

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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

The oxidoreductase CLIC4 is required to maintain mitochondrial function and resistance to exogenous oxidants in breast cancer cells.

Project description:The oxidoreductase CLIC4 is required to maintain mitochondrial function and resistance to exogenous oxidants in breast cancer cells.

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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

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.

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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

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

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Exogenous oxidants activate nuclear factor kappa B through Toll-like receptor 4 stimulation to maintain inflammatory phenotype in macrophage.

Project description:Disturbances in redox equilibrium in tissue can lead to inflammatory state, which is a mediatory factor in many human diseases. The mechanism(s) by which exogenous oxidants may activate an inflammatory response is not fully understood. Emerging evidence suggests that oxidant-induced Toll-like receptor 4 (TLR4) activation plays a major role in "sterile" inflammation. In the present study, we used murine macrophage RAW-Blue cells, which are chromosomally integrated with secreted embryonic alkaline phosphatase (SEAP) inducible by NF-?B. We confirmed the expression of TLR4 mRNA and protein in RAW-Blue cells by RT-PCR and Western blot, respectively. We showed that oxidants increased intracellular reactive oxygen species production and lipid peroxidation, which resulted in decreased intracellular total antioxidant capacity. Consistent with the actions of TLR4-specific agonist LPS-EK, exogenous oxidants increased transcriptional activity of NF-?B p65 with subsequent release of NF-?B reporter gene SEAP. These effects were blocked by pretreatment with TLR4 neutralizing pAb and TLR4 signaling inhibitor CLI-095. In addition, oxidants decreased the expression of I?B? with enhanced phosphorylation at the Tyr42 residue. Finally, oxidants and LPS-EK increased TNF? production, but did not affect IL-10 production, which may cause imbalance between pro- and anti-inflammatory processes, which CLI-095 inhibited. For biological relevance, we confirmed that oxidants increased release of TNF? and IL-6 in primary macrophages derived from TLR4-WT and TLR4-KO mice. Our results support the involvement of TLR4 mediated oxidant-induced inflammatory phenotype through NF-?B activation in macrophages. Thus exogenous oxidants may play a role in activating inflammatory phenotypes that propagate and maintain chronic disease states.

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

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

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Host CLIC4 is essential for breast cancer metastatic competence

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

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