The cell-intrinsic role of ANXA1 in human ILC2s
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE212517 | GEO | 2023/09/01
REPOSITORIES: GEO
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Project description:The cell-intrinsic role of ANXA1 in human ILC2s
| PRJNA875883 | ENA
Project description:A proteolytic cleavage experiment was performed with the recombinant unfolded protein Annexin A1 (ANXA1) and recombinant HTRA1_∆mac protease, to identify cleavage sites in ANXA1. In this experiment, unfolded and denatured ANXA1 was used to compare the cleavage sites that are cleaved efficiently and are surface exposed or not.
2024-09-20 | PXD031534 | Pride
Project description:Annexin 1 (ANXA1), an endogenous anti-inflammatory protein which modulates cellular processes such as proliferation, differentiation and apoptosis has been implicated in cancer initiation and progression. ANXA1 was previously shown to be regulated by hsa-miR-196a and promoted cell proliferation and anchorarge-dependent growth and suppressed apoptosis. However, whether ANXA1 itself regulates miRNA expression is unknown. Therefore, in this study, we investigated the regulation of miRNA by ANXA1 in breast cancer cells. Using microarray technology, 12 miRNAs were found to be significantly and consistently downregulated in MCF-7 cells (MCF-V5) overexpressing ANXA1 overexpressing MCF-7 cells (MCF-V5). Hsa-miR-26b* and hsa-miR-562 were chosen for further investigation.The data suggest that miR-26b* and miR-562 may play a role in ANXA1-induced migration and possibly angiogenesis by targeting NFKB and point towards a potential therapeutic target for breast cancer. Breast cancer MCF-7 cells (MCF-V5) overexpressing ANXA1 were cultured for RNA extraction and hybridization on Affymetrix miRNA microarrays. These were compared against the control, which were MCF-7 cells (MCF-EV) carrying an empty expression vector. Expression analyses were carried out in triplicates
2015-01-05 | E-GEOD-54439 | biostudies-arrayexpress
Project description:Annexin 1 (ANXA1), an endogenous anti-inflammatory protein which modulates cellular processes such as proliferation, differentiation and apoptosis has been implicated in cancer initiation and progression. ANXA1 was previously shown to be regulated by hsa-miR-196a and promoted cell proliferation and anchorarge-dependent growth and suppressed apoptosis. However, whether ANXA1 itself regulates miRNA expression is unknown. Therefore, in this study, we investigated the regulation of miRNA by ANXA1 in breast cancer cells. Using microarray technology, 12 miRNAs were found to be significantly and consistently downregulated in MCF-7 cells (MCF-V5) overexpressing ANXA1 overexpressing MCF-7 cells (MCF-V5). Hsa-miR-26b* and hsa-miR-562 were chosen for further investigation.The data suggest that miR-26b* and miR-562 may play a role in ANXA1-induced migration and possibly angiogenesis by targeting NFKB and point towards a potential therapeutic target for breast cancer.
2015-01-05 | GSE54439 | GEO
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
Project description:We analyzed the total proteome of group 2 innate lymphoid cells (ILC2s) after different stimulation with interleukin-33 (IL-33), a cytokine playing a critical role in human asthma, and TL1A, a TNF-family cytokine also known to activate ILC2s. Upon combined stimulation with IL-33 plus TL1A, we show that lung ILC2s produce high amounts of IL-9 and acquire a transient ‘ILC9’ phenotype. This phenotype is characterized by simultaneous production of large amounts of type 2 cytokines (IL-5, IL-13 and IL-9), induction of the IL-2 receptor CD25 (Il2ra), and of the transcription factors IRF4, JunB and BATF, that form immune-specific complexes known to induce IL-9 expression.
2024-03-05 | PXD041987 | Pride
Project description:Group 2 innate lymphoid cells (ILC2s) in the lung are stimulated by inhaled allergens. ILC2s do not directly recognize allergens but they are stimulated by cytokines including interleukin (IL)-33 released by damaged epithelium.Lung ILC2s, upon stimulation, produce T helper 2 cell-type cytokines inducing T cell independent allergic lung inflammation. We now report that lung ILC2s, upon activation by an allergen or IL-33, acquire the properties of memory cells. The activated ILC2s initially proliferate and secrete cytokines, followed by a contraction phase as they stop producing cytokines. Nevertheless, some persist long after the resolution of the inflammation and acquire intrinsic capacities to react to unrelated allergens more vigorously than naïve ILC2s, thus mediating a severe allergic lung inflammation. Gene expression profiles of the previously activated ILC2s show a gene signature of memory T cells. These antigen non-specific memory ILC2s may explain why asthma patients are often sensitized to multiple allergens. ILC2s were isolated from mouse lungs from naive and IL-33 injected mice 4 days, 14 days and 4 months after the initial treatment. RNA was extracted from those ILC2 populations and analyzed for gene expression profiles. RNA was also extracted from ILC2s isolated from lung draining mediastinal lymph node (mLN) 4 days and 14 days after IL-33 treatment.
2016-06-30 | E-GEOD-81700 | biostudies-arrayexpress
Project description:Transcriptomal comparison between group 2 innate lymphoid cells (ILC2s) in the murine small intestine (SI-ILC2s) and those in white adipose tissue (WAT-ILC2s).
2019-07-02 | GSE130530 | GEO
Project description:Annexin A1 (ANXA1) is a Ca2+-binding protein involved in pancreatic cancer (PC) progression. It is able to mediate cytoskeletal organization maintaining a malignant phenotype. ANXA1 Knock-Out (KO) MIA PaCa-2 cells partially lost their migratory and invasive capabilities and also the metastatization process is affected in vivo. Here, we investigated the microRNA (miRNA) profile in ANXA1 KO cells. The analysis of the modification in miRNA expression remarked the significant involvement of ANXA1 in PC progression. In this study, we focused on miR-196a which is a well known oncogenic factor in several tumour models and it appeared down-modulated in absence of ANXA1. Furthermore, both ANXA1 and miR-196a are able to trigger the mechanisms of the epithelial to mesenchymal transition (EMT). Our results show that the reintroduction of miR-196a through the mimic sequence restored the early aggressive phenotype of MIA PaCa-2. Then, ANXA1 seems to support the expression of miR-196a and its role. On the other hand, this miRNA is able to mediate some of protein functions in PC progression. This work elucidates the correlation between ANXA1 and specific miRNA sequences, particularly miR-196a, and provides new knowledge about the protein intracellular role.
2018-08-31 | E-MTAB-6599 | biostudies-arrayexpress
Project description:<p>Annexin A1 (AnxA1) is an anti-inflammatory protein present in different cells in biological systems, especially expressed in macrophages and neutrophils. Since neutrophils play an important role in infections and inflammatory processes and the AnxA1 and its relation in Candida spp. infections is not well understood, our study highlights a perspective in AnxA1 as a target protein in control the immune response during fungi infection. C57BL/6 wild-type (WT) and AnxA1 knockout (AnxA1-/-) peritoneal neutrophils were coinfected with Candida albicans or Candida auris for 4 hours. High levels of COX-2 were observed in WT and AnxA1-/- neutrophils infected with C. albicans and C. auris coinfection. In addition, AnxA1-/- neutrophils exhibited a marked increase of phosphorylated ERK, p-38 and JNK levels after coinfection with both Candida spp. Lipidomics approach shows that lack of AnxA1 produced a marked difference in lipid profile of control or coinfected neutrophil supernatants compared to WT, especially glycerophospholipids and glycerolipids. In summary, our results showed that endogenous AnxA1 regulates neutrophil response under fungal infection and its lipid membrane organization and metabolism. </p>
2021-12-03 | MTBLS2288 | MetaboLights