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Annexin 10 promotes invasion in QBC-939 cell

ABSTRACT: Annexin family is the largest category of eukaryotic calcium and phospholipid-binding proteins and plays important roles in various physiological processes, including cell differentiation and proliferation. More than 160 Annexin proteins are classified into 65 different speciesAs a new member of Annexin family, the role of ANXA10 in cancer progression is rarely investigated, and its expression and function in CCA need more experiments to reveal.

ORGANISM(S): Homo sapiens

PROVIDER: GSE132279 | GEO | 2022/05/17

REPOSITORIES: GEO

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ANXA10 Promotes Melanoma Metastasis by Suppressing the Ubiquitination of PKD1 Mediated by E3 Ligase TRIM41

Project description:Melanoma is a highly metastatic type of cancer which requires novel and effective targeted therapies. Annexin A10 (ANXA10), a member of annexin family, is a calcium and phospholipid binding protein. Considerable evidences indicate that ANXA10 is involved in tumor progression, but little is known about the involvement of ANXA10 in melanoma. In this study, we reported that ANXA10 expression was significantly up-regulated and correlated with melanoma progression. Knockout of ANXA10 profoundly reduced cell migration and metastatic activity of melanoma. Mechanistic investigations showed that ANXA10 knockout induced N- to E-cadherin switch by upregulating SMAD6, an inhibitory SMAD in TGF-β/ SMAD pathway. The negative regulation of ANXA10 on SMAD6 was dependent on PKD1. We demonstrated that ANXA10 interacted with PKD1 and inhibited E3 ligase TRIM41-mediated PKD1 degradation. In B16F10 melanoma cells, the protein levels of ANXA10 and PKD1 were negatively correlated with SMAD6, but positively related to cell migration. In addition, a negative correlation of ANXA10 and SMAD6 levels was also observed in clinical samples, which was associated with melanoma progression. Our findings suggest that ANXA10/PKD1/ SMAD6 axis might be new targets of therapeutic strategies for melanoma metastasis.

2021-05-20 | GSE174724 | GEO

Annexin A3 is necessary for artery-vein alignment in the mouse retinas (RNA-seq analysis of isolated retinal endothelial cells from Anxa3;Tie2-cre mutant mice)

Project description:Annexin A3 (Anxa3) is a member of the calcium-regulated, cell membrane binding family of Annexin proteins. We previously confirmed that Anxa3 is expressed in the endothelial lineage in vertebrates and that loss of Anxa3 in Xenopus laevis leads to embryonic blood vessel defects. However, the biological function of Anxa3 in mammals is completely unknown. In order to investigate Anxa3 vascular function in mammals, we generated an endothelial cell specific Anxa3 conditional knockout mouse model (Anxa3f/f;Tie2-Cre).

2019-08-08 | GSE135528 | GEO

Role of annexin A2 in muscle repair

Project description:Repair of injured muscle involves repair of injured myofibers through the involvement of dysferlin and its interacting partners, including annexin. Studies with mice and patients have established that dysferlin deficit leads to chronic inflammation and adipogenic replacement of the diseased muscle. However, longitudinal analysis of annexin deficit on muscle pathology and function is lacking. Here we show that unlike annexin A1, but similar to dysferlin, lack of annexin A2 (AnxA2) causes poor myofiber repair and progressive weakening with age. However, unlike dysferlin-deficient muscle, AnxA2-deficient muscles do not exhibit chronic inflammation or adipogenic replacement. Deletion of AnxA2 in dysferlin deficient mice reduces inflammation, adipogenic replacement, and loss in muscle function caused by dysferlin deficit. These results show that: a) AnxA2 facilitates myofiber repair, b) chronic inflammation and adipogenic replacement of dysferlinopathic muscle requires AnxA2, and c) inhibiting AnxA2-mediated inflammation is a novel therapeutic avenue for dysferlinopathy.

2016-10-04 | GSE87557 | GEO

Annexin A1 exerts renoprotective effects in experimental crescentic glomerulonephritis

Project description:The glucocorticoid-inducible protein annexin A1 has been shown to function as key-regulator of the resolution phase of inflammation but its role in immune-mediated crescentic glomerulonephritis has not been studied so far. Acute crescentic glomerulonephritis was induced in annexin A1 deficient and wildtype mice using a sheep serum against rat glomerular basement membrane constituents. Alterations in gene expression were determined by RNA-Seq and gene ontology analysis. Intrinsic annexin A1 has a protective effect in reducing pro-inflammatory signals and infiltration of neutrophil granulocytes during crescentic GN. The annexin A1 signaling cascade may therefore provide novel targets for the treatment of inflammatory kidney disease.

2022-10-04 | GSE204873 | GEO

Transcription profiling by array of human breast cancer cell line BT-474 with annexin A1 over-expression or silenced with siRNA to demonstrate design of multi-condition experiments

Project description:Multiple-condition experiment was desinged to be any number of conditions in an experiment without replicate observations for microarray and used to identify genes differentially expressed between different pairs of conditions (treatments).<br> In this study we used breast cancer stable cell lines for overexpressing and silencing annexin A1 (ANXA1), which belongs to a family of -dependent phospholipid binding proteins and are preferentially located on the cytosolic face of the plasma membrane. Cell lines overexpressing ANXA1 (MDA_MB-453/cDNA) were generated by introducing retroviral vectors containing ANXA1 cDNA (pBabe/ANXA1 cDNA) into breast cancer cell line MDA-MB-453 (a low expressor of ANXA1). Breast cancer cell line BT-474, a high expressor of ANXA1, was infected with ANXA1 siRNA-plasmid viruses to knockdown ANAXAI expressor (BT-474/siRNA) where nucleotides corresponding to siRNA were synthesized and ligated into the pLNCX retroviral vector [35,36]. We also used a pLNCX/U6 empty vector to infect BT-474 and obtained an empty vector expressor. Therefore, 5 breast cancer cell lines (MDA_MB-453, MDA_MB-453/cDNA, BT-474, BT-474/siRNA, and BT-474/U6) are attributed to two genotypes: MDA_MB-453 and BT-474. MCE was performed for microarray analysis with these 5 breast cancer cell lines, that is, only one sample was drawn from each breast cancer cell line.

2010-06-26 | E-MEXP-2775 | biostudies-arrayexpress

Regulation of somatosensory mechanotransduction by Annexin A6

Project description:Sensory neuron mechanically-activated slowly adapting currents have been linked to noxious mechanosensation. We identified a Conotoxin, Noxious Mechanosensation Blocker -1, that blocks such currents selectively. Using an active biotinylated form of the toxin we identified 67 binding proteins in sensory neurons and sensory neuron-derived cell lines using mass spectrometry. Annexin A6 was the most frequently identified binding protein. Annexin A6 knockout mice showed an enhanced sensitivity to mechanical stimuli. Rapidly adapting currents were enhanced and slowly adapting channels diminished. The percentage of neurons expressing slowly adapting currents fell and non-responsive neurons increased. Conversely, overexpression of annexin A6 in DRG neurons inhibited rapidly adapting currents without effects on slowly adapting currents. Co-expression of annexin A6 with Piezo 2 led to an inhibition of Piezo-mediated rapidly adapting currents. AAV-mediated gene delivery of annexin A6 to sensory neurons in a mouse model of osteoarthritis attenuated mechanical pain. These data demonstrate a role for annexin A6 in somatosensory mechanotransduction.

2018-04-17 | PXD005718 | Pride

Annexin A8 deficiency delayed atherosclerosis progression

Project description:Annexin A8 deficiency delayed atherosclerosis progression

| PRJNA855372 | ENA

Dynamic response of annexin A11-associated gene expression to cisplatin treatment

Project description:Based on a time-course study of cisplatin response in ovarian cancer cells with/without suppression of annexin A11 expression using whole genome oligonucleotide microarrays, we identified a set of differentially expressed genes associated with annexin A11 expression and patterns of gene expressions in response to cisplatin exposure. Keywords: human ovarian cancer cell lines

2009-12-01 | GSE13893 | GEO

Investigation of over-expressing Annexin receptor cell line with and without agonists

Project description:The therapeutic potential of pro-resolution factors in determining the outcome of inflammatory events has gained ground over the past decade. However, the attention has been focused on the non-genomic effects of these endogenous, anti-inflammatory substances. In this study, we have focused our attention on identifying specific annexin 1 (AnxA1) protein/ALX receptor mediated gene activation, in an effort to identify down-stream genomic targets of this well-known, glucocorticoid induced, pro-resolution factor. In this study, we used four different types of samples (with 2 replicates each):1)cells transfected with the empty pGEX-4T-327 vector and vehicle (PBS) treated; 2)cells transfected with the annexin receptor ALXR (also known as FPR2) and vehicle (PBS) treated; 3)cells transfected with the annexin receptor ALXR and treated with 10uM Ac-26 peptide for 4 hours; 4) cells transfected with the annexin receptor ALXR and treated with 0.5uM Annexin 1 for 4 hours. After the treatments, cells were collected for RNA extraction.

2010-09-28 | E-GEOD-14807 | biostudies-arrayexpress

Binding partners of Annexin A2 in MDA-MB-231 cells

Project description:A mass-spec of proteins found bound to Annexin A2 following a immunoprecipitation of Annexin A2 from cell lysate of MDAMB231 cells plated 1) on plastic or 2) on collagen-1

2023-10-11 | MSV000093084 | MassIVE

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