Dynamic expression of CD9 protein in T-cell acute lymphoblastic leukemia [bulk RNA-seq]
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE319183 | GEO | 2026/04/27
REPOSITORIES: GEO
Similar Datasets
Project description:Transcriptomes of differentiated cells of the conditionally immortalized mouse podocyte cell line SVI (Schiwek et al., Kidney Int. 66: 91-101, 2004) were determined as described in Warsow et al. (Kidney Int. 84: 104-115, 2013) after application of mechanical stress (Endlich et al., J. Am. Soc. Nephrol. 12: 413-422, 2001) as compared to control conditions. Elevated glomerular pressure represents a high risk for the development of severe kidney diseases and causes an increase of mechanical load to podocytes. In this study we investigated whether mechanical stress alters gene expression in cultured podocytes using gene arrays. We found that tetraspanin CD9 is significantly upregulated in cultured podocytes after mechanical stress. The differential expression of CD9 was confirmed by RT-PCR and Western blot under stretched and unstretched conditions. Furthermore, mechanical stress resulted in a relocalization of CD9. To get an insight into the functional role of CD9, podocytes were transfected with pEGFP-CD9. The expression of CD9 induced the formation of substratum-attached thin arborized protrusions (TAPs). Ca2+ depletion revealed that podocytes over-expressing CD9 possess altered adhesive properties in contrast to the control transfected cells. Finally, elevated CD9 expression increased migration of podocytes in a wound assay. In summary, our results suggest that upregulation of CD9 may play an important role in podocyte morphology, adhesion and migration. Three independent batches were used.
2015-02-27 | E-GEOD-66336 | biostudies-arrayexpress
Project description:Transcriptomes of differentiated cells of the conditionally immortalized mouse podocyte cell line SVI (Schiwek et al., Kidney Int. 66: 91-101, 2004) were determined as described in Warsow et al. (Kidney Int. 84: 104-115, 2013) after application of mechanical stress (Endlich et al., J. Am. Soc. Nephrol. 12: 413-422, 2001) as compared to control conditions. Elevated glomerular pressure represents a high risk for the development of severe kidney diseases and causes an increase of mechanical load to podocytes. In this study we investigated whether mechanical stress alters gene expression in cultured podocytes using gene arrays. We found that tetraspanin CD9 is significantly upregulated in cultured podocytes after mechanical stress. The differential expression of CD9 was confirmed by RT-PCR and Western blot under stretched and unstretched conditions. Furthermore, mechanical stress resulted in a relocalization of CD9. To get an insight into the functional role of CD9, podocytes were transfected with pEGFP-CD9. The expression of CD9 induced the formation of substratum-attached thin arborized protrusions (TAPs). Ca2+ depletion revealed that podocytes over-expressing CD9 possess altered adhesive properties in contrast to the control transfected cells. Finally, elevated CD9 expression increased migration of podocytes in a wound assay. In summary, our results suggest that upregulation of CD9 may play an important role in podocyte morphology, adhesion and migration.
2015-02-27 | GSE66336 | GEO
Project description:Vascular smooth muscle cell (VSMC) migration and proliferation are critical events in the development of neointima following vascular injury. Exogenous expression of human CD9 by CD9-adenoviral transduction led to increases in neointima. CD9 expression significantly augmented PI-3 kinase dependent Akt phosphorylation with concurrent adhesion to extracellular matrix protein fibronectin (FN). Furthermore,enhanced Akt phosphorylation was attenuated by anti-CD9 mAb7 binding. As multiple factors contribute to the regulation of VSMC phenotype, our aim was to establish whether increased CD9 expression would induce changes in the expression of other genes associated with VSMC proliferation and motility. RASM were transduced with either CD9 adenovirus or control and were plated on FN for 6hours. Cells were harvested from 3 replicate plates and total RNA from each was isolated using the TRIzol method and pooled for each CD9 and LacZ transduced RASM. RNA was sent to Genome Explorations Memphis TN for microarray analysis. Microarray analyses were done using the U230.2 rat gene chip from Affymetrix using RNA prepared from two RASM transduction experiments. Two independent microarray data sets have been generated and analyzed by comparing the filtered gene lists generated by the Affymetrix GeneChip Operating Software and looking for regulated genes common both sets of data. Analysis of this data showed the regulation of some key genes involved in the modulation of VSMC motility and proliferation. Keywords: vascular smooth muscle cells, vascular injury, tetraspanin, proliferation, neointima, motility, fibronectin (FN), rat aortic smooth muscle (RASM)
2009-11-12 | GSE13594 | GEO
Project description:In order to identify state changes that mediate the transition from sensitive to a resistant cell states, we applied RNA velocity analysis to an existing single-cell RNAseq (scRNAseq) dataset of BRD4 inhibitor sensitive and resistant SUM149 and SUM159 triple negative breast cancer cell lines. Both SUM149 and SUM159 cell lines treated with or without JQ1 had similar cell communities and trajectories including a stem cell-like and embryonic diapause (SCLED) cell state, a transiting cell state and a number of drug resistant states. Interestingly a transcriptional signature derived from the transiting state but not the SCLED state was associated with worsened outcomes in basal-like breast cancer patients as well as with a micrometastasis signature suggesting that the ability to transit from the SCLED state to drug resistant states could contribute to patient outcomes. The shift from the SCLED state to a transiting cell state was characterized by elevated expression of the CD9 tetraspanin. CD9 knockdown sensitized SUM149 tumor cells to JQ1 in vitro and in vivo trapping cells in the SCLED state and limiting transit to resistant cell states. CD9 knockdown sensitized SUM149 to multiple additional cytotoxic drugs suggesting a generalized role in drug resistance. Thus, CD9 appears to be critical for the ability of triple negative breast cancer cells to escape from a stem cell-like/embryonic diapause state and transition into a treatment resistant state.
2022-08-25 | GSE196952 | GEO
Project description:Clostridioides difficile CD9 Genome sequencing and assembly
| PRJNA85681 | ENA
Project description:The tetraspanins CD9, CD81, and CD63 are among the most widely used markers of Extracellular Vesicles (EVs) and are also used to isolate the vesicles they decorate. If their function in EVs is largely unknown, they have been suggested to play a role in the sorting of protein cargos into EVs or to regulate the uptake of EVs by acceptor cells. Using different tetraspanin-deficient MCF7 breast cancer cell lines, we have shown that the absence of any of these 3 tetraspanins had a minimal impact on their protein composition, as analyzed by label-free quantitative mass spectrometry. However, the EVs released by cells deficient in both CD9 and CD81 showed a decrease level of CD9P-1/EWI-F and EWI-2 (encoded by the genes PTGFRN and IGSF8 respectively), which are two well-characterized CD9 and CD81 molecular partners.
2023-08-03 | PXD042940 | Pride
Project description:Epithelial colonisation is often a critical first step in bacterial pathogenesis, however, different bacterial species utilise several different receptors at the cell membrane interface to adhere to cells. We have previously demonstrated that interference of the human tetraspanin, CD9, can reduce adherence of multiple species of bacteria to epithelial cells by approximately 50%. However, CD9 does not act as a receptor and is responsible for organising and clustering partner proteins commandeered by bacteria for efficient adherence. CD9 can organise numerous host proteins at the cell membrane but the full interactome has not been delineated. Using a novel CD9 proximity-labelling model, we describe a diverse CD9 interactome with 1,837 significantly enriched proteins over four hours. These putative proximal proteins are associated with various cellular pathways including cell adhesion, ECM-receptor interactions, endocytosis, SNARE interactions and adherens and tight junctions. Significant and known interactors of CD9 were enriched including β1 integrins and major immunoglobulin superfamily members but also included several known bacterial adherence receptors including CD44, CD46 and CD147. We further demonstrate dynamism of the interactome during infection at three separate time points with two different bacterial species, Neisseria meningitidis and Staphylococcus aureus. During meningococcal infection, we observed 13 unique significantly enriched proximal proteins associated with CD9 across four hours compared to uninfected cells. However, upon staphylococcal far fewer enriched proximal proteins were identified demonstrating that different bacteria require different host factors during CD9-mediated bacterial adherence. Transient knockdown of CD44 and CD147, candidate receptor proteins identified in our screen, significantly reduced staphylococcal and meningococcal adherence respectively. This effect was ablated in the absence of CD9 or if epithelial cells were treated with a CD9-derived peptide demonstrating the association of these proteins during staphylococcal and meningococcal adherence. We demonstrate for the first time the CD9 interactome of epithelial cells and that bacteria hijack these interactions to efficiently adhere to epithelial cells. This process is bacterial species specific, recruiting a number of different proteins during infection but a host-derived peptide is able to interfere with this process. We have therefore developed a tool that can measure changes within the CD9 interactome after cellular challenge, established a mechanism in which CD9 is used as a universal organiser of bacterial adhesion platforms and demonstrated that this process can be stopped using a CD9-derived peptide.
2025-10-28 | PXD058283 | Pride
Project description:Epithelial colonisation is often a critical first step in bacterial pathogenesis, however, different bacterial species utilise several different receptors at the cell membrane interface to adhere to cells. We have previously demonstrated that interference of the human tetraspanin, CD9, can reduce adherence of multiple species of bacteria to epithelial cells by approximately 50%. However, CD9 does not act as a receptor and is responsible for organising and clustering partner proteins commandeered by bacteria for efficient adherence. CD9 can organise numerous host proteins at the cell membrane but the full interactome has not been delineated. Using a novel CD9 proximity-labelling model, we describe a diverse CD9 interactome with 1,837 significantly enriched proteins over four hours. These putative proximal proteins are associated with various cellular pathways including cell adhesion, ECM-receptor interactions, endocytosis, SNARE interactions and adherens and tight junctions. Significant and known interactors of CD9 were enriched including β1 integrins and major immunoglobulin superfamily members but also included several known bacterial adherence receptors including CD44, CD46 and CD147. We further demonstrate dynamism of the interactome during infection at three separate time points with two different bacterial species, Neisseria meningitidis and Staphylococcus aureus. During meningococcal infection, we observed 13 unique significantly enriched proximal proteins associated with CD9 across four hours compared to uninfected cells. However, upon staphylococcal far fewer enriched proximal proteins were identified demonstrating that different bacteria require different host factors during CD9-mediated bacterial adherence. Transient knockdown of CD44 and CD147, candidate receptor proteins identified in our screen, significantly reduced staphylococcal and meningococcal adherence respectively. This effect was ablated in the absence of CD9 or if epithelial cells were treated with a CD9-derived peptide demonstrating the association of these proteins during staphylococcal and meningococcal adherence. We demonstrate for the first time the CD9 interactome of epithelial cells and that bacteria hijack these interactions to efficiently adhere to epithelial cells. This process is bacterial species specific, recruiting a number of different proteins during infection but a host-derived peptide is able to interfere with this process. We have therefore developed a tool that can measure changes within the CD9 interactome after cellular challenge, established a mechanism in which CD9 is used as a universal organiser of bacterial adhesion platforms and demonstrated that this process can be stopped using a CD9-derived peptide.
2025-10-28 | PXD067302 | Pride
Project description:Dysfunctional white adipose tissue contributes to the development of obesity-related morbidities, including insulin resistance, dyslipidemia, and other metabolic disorders. Adipose tissue macrophages (ATMs) accumulate in obesity and play both beneficial and harmful roles in the maintenance of adipose tissue homeostasis and function. Despite their importance, the molecules and mechanisms that regulate these diverse functions are not well understood. Lipid-associated macrophages (LAMs), the dominant subset of obesity-associated ATMs, accumulate in crown-like structures and are characterized by a metabolically activated and proinflammatory phenotype. We previously identified CD9 as a surface marker of LAMs. However, the contribution of CD9 to the activation and function of LAMs during obesity is unknown. Using a myeloid-specific CD9 knockout model, we show that CD9 supports ATM-adipocyte adhesion and crown-like structure formation. Furthermore, CD9 promotes the expression of pro-fibrotic and extracellular matrix remodeling genes. Loss of myeloid CD9 reduces adipose tissue fibrosis, increases visceral adipose tissue accumulation, and improves global metabolic outcomes during diet-induced obesity. These results identify CD9 as a causal regulator of pathogenic LAM functions, highlighting CD9 as a potential therapeutic target for treating obesity-associated metabolic disease.
2026-01-20 | GSE311351 | GEO
Project description:Bromo- and extra-terminal domain (BET) inhibitors (BETi) have been shown to decrease tumor growth in preclinical models and clinical trials. However, toxicity and rapid emergence of resistance have limited their clinical implementation. To identify state changes underlying acquisition of resistance to the JQ1 BETi, we reanalyzed single-cell RNAseq data from JQ1 sensitive and resistant SUM149 and SUM159 triple negative breast cancer cell lines. Parental and JQ1-resistant SUM149 and SUM159 exhibited a stem cell-like and embryonic diapause (SCLED) cell state as well as a transitional cell state between the SCLED state existing both treatment naïve and treated cells, and a number of JQ1 resistant cell states. A transitional cell state transcriptional signature but not a SCLED state transcriptional signature predicted worsened outcomes in basal-like breast cancer patients suggesting that transit from the SCLED state to drug resistant states contributes to patient outcomes. Entry of SUM149 and SUM159 into the transitional cell state was characterized by elevated expression of the CD9 tetraspanin. Knockdown or inhibition of CD9 sensitized cells to multiple targeted and cytotoxic drugs in vitro. Importantly, CD9 knockdown or blockade sensitized SUM149 to JQ1 in vivo by trapping cells in the SCLED state and limiting transit to resistant cell states. Thus, CD9 appears to be critical for transition from a SCLED state into treatment resistant cell states and warrants exploration as a therapeutic target in basal-like breast cancer.
2023-06-01 | GSE221183 | GEO