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Gene expression analysis of liver and heart from wildtype and ABCB5 mutant mice

ABSTRACT: Abcb5 is a member of the ATP-Binding Cassette (ABC) transporter superfamily. It is an energy dependent transporter and its role is unknown yet. We are characterizing this transporter at the genomic and protein level. We know that it is highly expressed in pigmented cells, including pigmented cells of the CNS (retinal pigment epithelium and basal ganglion cells). We found it highly expressed in melanotic melanoma and in alveolar soft part sarcoma.

ORGANISM(S): Mus musculus

PROVIDER: GSE57699 | GEO | 2024/12/01

REPOSITORIES: GEO

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The stem cell gene ABCB5 mediates cancer resistance to apoptosis

Project description:Cancer stem cells (CSC) responsible for disease progression and therapeutic resistance have been identified in several human malignancies, including colorectal cancer (CRC). However, the molecular mechanisms through which CSC drive tumor growth are incompletely understood. ABCB5, a member of the ATP-binding cassette superfamily of active transporters, serves as a CSC-specific multidrug resistance mechanism in diverse human malignancies. Additionally, ABCB5 has recently been demonstrated to function as an anti-apoptotic gene in tissue-specific non-malignant stem cells. Here we demonstrate that ABCB5 also serves an anti-apoptotic role required for CSC maintenance in human cancer. Targeted inhibition of ABCB5, previously shown to be preferentially expressed on CD133-positive CRC stem cells, induced tumor cell apoptosis in vitro and in vivo and inhibited human CRC growth in NSG recipient mice. Mechanistically, ABCB5-positive tumor cell ablation through monoclonal antibody-mediated blockade or shRNA-mediated gene knockdown resulted in diminished production of the receptor tyrosine kinase AXL, a pro-tumorigenic molecule identified herein to be preferentially produced by CRC stem cells. Restoration of AXL expression through gene transfection in ABCB5 knockdown tumors partially restored tumor growth, demonstrating that ABCB5-positive CRC stem cells drive tumorigenicity at least in part through production of AXL. Our results establish a novel anti-apoptotic function of ABCB5 in human cancer and indicate that targeted blockade of ABCB5 represents a novel strategy for CSC eradication, independent of its previously established function as a multidrug resistance mediator.

2018-08-01 | GSE71670 | GEO

Expression data from ABCB5-positive and ABCB5-negative GBM cells

Project description:We analyzed, by HTA 2.0, the GBM cell lines LN-18, LN-229, and U-87 MG after fluoresence-activated cell sorting (FACS) into ABCB5+ and ABCB5- fractions. Poor prognosis associated with glioblastoma multiforme (GBM) results from tumor resistance to therapy and high rate of recurrence. Compelling evidence suggests this is driven by subpopulations of slow-proliferating cancer stem cells with tumor-initiating potential. ATP-binding cassette member B5 (ABCB5) has been identified as a molecular marker for distinct subsets of chemoresistant tumor-initiating cell populations in diverse human malignancies. In the current study, we examined the potential role of ABCB5 in growth and chemoresistance of GBM. We found ABCB5 to be preferentially expressed in clinical GBM tumors and co-expressed with the stem cell marker CD133 in subpopulations of human GBM cell lines U-87 MG, LN-18 and LN-229. Antibody-mediated functional ABCB5 blockade inhibited proliferation and survival of human GBM cells and sensitized them to temozolomide (TMZ)-induced apoptosis. Likewise, in an in vivo GBM xenograft study in immunodeficient mice, anti-ABCB5 monoclonal antibody treatment inhibited tumor growth and sensitized tumors to TMZ therapy. Mechanistically, we demonstrated that ABCB5 regulates cell cycle checkpoint molecules to revoke drug-induced G2-M arrest and augments drug-mediated cell death. Overall, our data establish ABCB5 as a marker of GBM chemoresistance and point to the potential of ABCB5 targeting in improvement of current GBM therapies.

2020-03-05 | GSE127895 | GEO

ABCB5 is activated by MITF and b-catenin and is associated with melanoma differentiation

Project description:Defining markers of different phenotypic states in melanoma is important for understanding disease progression, determining the response to therapy, and defining the molecular mechanisms underpinning phenotype-switching driven by the changing intratumor microenvironment. The ABCB5 transporter is implicated in drug-resistance and has been identified as a marker of melanoma-initiating cells. Indeed, ongoing studies are using ABCB5 to define stem cell populations. However, we show here that the ABCB5 is a direct target for the Microphthalmia-associated transcription factor MITF and its expression can be induced by b-catenin, a key activator and co-factor for MITF. Consequently, ABCB5 mRNA expression is primarily associated with melanoma cells exhibiting differentiation markers. The results suggest first that ABCB5 is unlikely to represent a marker of dedifferentiated melanoma stem cells, and second that ABCB5 may contribute to the non-genetic drug-resistance associated with highly differentiated melanoma cells. To reconcile the apparently conflicting observations in the field we propose a model in which ABCB5 may mark a slow-cycling differentiated population of melanoma cells.

2019-10-16 | GSE136803 | GEO

Functional analysis of ABCB5 in melanoma cells

Project description:Functional analysis of ABCB5 in A375 and G3361 melanoma cells, by comparing stably-transfected controls to ABCB5-shRNA-targeted cells. 12 samples total. Replicates n=3 for the following 4 groups: A375 pSUPER-retro-puro-Vector vs. A375 pSUPER-retro-puro-ABCB5-KD; G3361 pSUPER-retro-puro-shCNTRL vs. G3361 pSUPER-retro-puro-ABCB5-KD.

2014-06-17 | E-GEOD-38290 | biostudies-arrayexpress

Genome-wide expression microarray data of MCSP- and ABCB5-enriched CTCs

Project description:Circulating Tumour Cells (CTCs) act as tumour seeds for haematogeneous melanoma spread of melanoma. Since CTCs have been reported to be heterogeneous in melanoma, the characterisation of the different melanoma CTC subpopulations harbours biological and clinical significance. For detection of melanoma CTCs, melanoma-associated markers (i.e. MCSP, melanoma-associated chondroitin sulphate proteoglycan) have been used; however, recent studies have found that melanoma CTCs commonly express ABCB5 (ATP-binding cassette sub-family B member 5) a melanoma-initiating marker. Here, we used a genome-wide expression microarray to interrogate the transcriptome of MCSP-enriched and ABCB5-enriched CTC fraction in order to provide a better understanding of their biology and role in melanoma metastasis. Findings from this study highlited the distinct transcriptional programming of both CTC subpopulations.

2018-05-11 | GSE113166 | GEO

Newly defined ABCB5+ dermal mesenchymal stem cells promote healing of chronic iron overload wounds via secretion of interleukin-1 receptor antagonist

Project description:Here we report the beneficial effects of a newly identified dermal cell subpopulation expressing the ATP-binding cassette subfamily B member 5 (ABCB5) for the therapy of non-healing wounds. Local administration of dermal ABCB5+-derived MSCs attenuated macrophage-dominated inflammation and thereby accelerated healing of full-thickness excisional wounds in the iron overload mouse model mimicking the non-healing state of human venous leg ulcers. The observed beneficial effects were due to interleukin-1 receptor antagonist (IL-1RA) secreted by ABCB5+-derived MSCs, which dampened inflammation and shifted the prevalence of unrestrained pro-inflammatory M1 macrophages towards repair promoting anti-inflammatory M2 macrophages at the wound site. The beneficial anti-inflammatory effect of IL-1RA released from ABCB5+-derived MSCs on human wound macrophages was conserved in humanized NOD-scid IL2rγnull mice. In conclusion, human dermal ABCB5+ cells represent a novel, easy accessible and marker-enriched source of MSCs which holds substantial promise to successfully treat chronic non-healing wounds in humans.

2019-01-30 | GSE125829 | GEO

Functional analysis of ABCB5 in melanoma cells

Project description:Functional analysis of ABCB5 in A375 and G3361 melanoma cells, by comparing stably-transfected controls to ABCB5-shRNA-targeted cells.

2014-06-17 | GSE38290 | GEO

ABCB5+ limbal epithelial stem cells inhibit developmental, but promote inflammatory (lymph)angiogenesis while preventing corneal inflammation

Project description:ABCB5 is marker for Limbal epithilal stem cells. A comparison between ABCB5+ versus ABCB5- cultured human limbal epithelial cells was carried out to evaluate the properties of the limbal stem cell ABCB5+ with a special focus on their role in inflammation and angiogenesis.

2023-10-24 | PXD041004 | Pride

Expression data from ABCB5-positive and ABCB5-negative GBM cells

Project description:Expression data from ABCB5-positive and ABCB5-negative GBM cells

| PRJNA525717 | ENA

Candida parapsilosis Mdr1B and Cdr1B are drivers of Mrr1-mediated clinical fluconazole resistance

Project description:Previous work has demonstrated that non-synonymous mutations in the gene encoding the putative transcription factor CpMrr1 can influence fluconazole susceptibility; however, the direct contribution of these mutations and how they influence fluconazole resistance in clinical isolates is poorly understood. We identified ten non-synonymous CpMRR1 mutations in a collection of 35 fluconazole resistant clinical isolates. The mutations leading to the A854V, R479K, and I283R substitutions were further examined and found to be activating mutations leading to increased fluconazole resistance. In addition to CpMDR1, we identified another major facilitator superfamily (MFS) transporter gene (CpMDR1B, CPAR2_603010) and an ATP-binding Cassette (ABC) transporter gene (CpCDR1B, CPAR2_304370), as being up-regulated in isolates carrying CpMRR1 activating mutations.

2022-04-18 | GSE196409 | GEO

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