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CLIC4 deficiency alters mitochondrial function and transcriptional profiles in murine 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: GSE173997 | GEO | 2022/09/14

REPOSITORIES: GEO

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

2022-07-15 | GSE188780 | 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.

2020-11-26 | GSE141057 | GEO

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 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.

| PRJNA727829 | ENA

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

2021-12-21 | GSE191077 | GEO

Host CLIC4 is essential for breast cancer metastatic competence

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

| PRJNA767846 | ENA

Sulfite Alters the Mitochondrial Network in Molybdenum Cofactor Deficiency.

Project description:Molybdenum cofactor deficiency (MoCD) is an autosomal recessive disorder belonging to the large family of inborn errors in metabolism. Patients typically present with encephalopathy and seizures early after birth and develop severe neurodegeneration within the first few weeks of life. The main pathomechanism underlying MoCD is the loss of function of sulfite oxidase (SO), a molybdenum cofactor (Moco) dependent enzyme located in mitochondrial intermembrane space. SO catalyzes the oxidation of sulfite (SO3 2-) to sulfate (SO4 2-) in the terminal reaction of cysteine catabolism, and in the absence of its activity, sulfurous compounds such as SO3 2-, S-sulfocysteine, and thiosulfate accumulate in patients. Despite growing evidence that these compounds affect neuronal and mitochondrial function, the molecular basis of neuronal dysfunction and cell death in MoCD is still poorly understood. Here we show that mitochondria are severely affected by the loss of SO activity. SO-deficient mouse embryonic fibroblasts display reduced growth rates and impaired ATP production when cultured in galactose, which is an indicator of mitochondrial dysfunction. We also found that mitochondria in SO-deficient cells form a highly interconnected network compared to controls while displaying a slight decrease in motility and unchanged mitochondrial mass. Moreover, we show that the mitochondrial network is directly influenced by SO3 2-, as a moderate elevation of SO3 2- lead to the formation of an interconnected mitochondrial network, while high SO3 2- levels induced fragmentation. Finally, we found a highly interconnected mitochondrial network in MoCD patient-derived fibroblasts, similar to our findings in mouse-derived fibroblasts. We therefore conclude that altered mitochondrial dynamics are an important contributor to the disease phenotype and suggest that MoCD should be included among the mitochondrial disorders.

| S-EPMC7817995 | biostudies-literature

CLIC4 localizes to mitochondrial-associated membranes and mediates cardioprotection.

Project description:Mitochondrial-associated membranes (MAMs) are known to modulate organellar and cellular functions and can subsequently affect pathophysiology including myocardial ischemia-reperfusion (IR) injury. Thus, identifying molecular targets in MAMs that regulate the outcome of IR injury will hold a key to efficient therapeutics. Here, we found chloride intracellular channel protein (CLIC4) presence in MAMs of cardiomyocytes and demonstrate its role in modulating ER and mitochondrial calcium homeostasis under physiological and pathological conditions. In a murine model, loss of CLIC4 increased myocardial infarction and substantially reduced cardiac function after IR injury. CLIC4 null cardiomyocytes showed increased apoptosis and mitochondrial dysfunction upon hypoxia-reoxygenation injury in comparison to wild-type cardiomyocytes. Overall, our results indicate that MAM-CLIC4 is a key mediator of cellular response to IR injury and therefore may have a potential implication on other pathophysiological processes.

| S-EPMC9586484 | biostudies-literature

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