Investigating TIAM1 in NSCLC (ChIP-Seq)
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PROVIDER: PRJNA906610 | ENA |
REPOSITORIES: ENA
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Project description:Investigating TIAM1 in NSCLC (RNA-Seq)
| PRJNA906609 | ENA
Project description:The T lymphoma invasion and metastasis inducing protein 1 (TIAM1) is a guanine nucleotide exchange factor (GEF) that activates the small GTPase RAC1. We have shown that nuclear TIAM1 promotes the migration of NSCLC cells and regulates the expression of adhesion genes as part of a repressive complex. To further investigate this, we performed ChIP-Seq analysis to determine the enrichment of TIAM1, TRIM28 and H3K9me3 to chromatin in H441 cells.
2023-09-12 | GSE219029 | GEO
Project description:The T lymphoma invasion and metastasis inducing protein 1 (TIAM1) is a guanine nucleotide exchange factor (GEF) that activates the small GTPase RAC1. We have shown that nuclear TIAM1promotes the migration of NSCLC cells. To investigate the requirement for TIAM1 in regulating gene expression of NSCLC cells, we performed RNA-seq on H441 cells transfected with either siRNA for TIAM1 (siTIAM1) or a control siRNA (siControl) to identify differentially expressed genes.
2023-09-12 | GSE219028 | GEO
Project description:The T lymphoma invasion and metastasis inducing protein 1 (TIAM1) is a guanine nucleotide exchange factor (GEF) that activates the small GTPase RAC1 and regulates a plethora of functions such as cell proliferation, migration, apoptosis and polarity. Recently, we demonstrated that TIAM1 shuttles between the cytoplasm and nucleus. Nuclear TIAM1 has an inhibitory role on TAZ transcriptional activity by impairing the interaction of TAZ with TEAD. To further demonstrate the inhibitory role of TIAM1 on TAZ we performed ChIP-Seq analysis to determine the enrichment of TAZ to chromatin of parental or CRISPR-mediated TIAM1 knockout SW480 cells.
2017-04-26 | GSE90490 | GEO
Project description:Lung cancer is the leading cause of cancer deaths. Its high mortality is associated with high metastatic potential. Here, we show that the RAC1-selective guanine nucleotide exchange factor T cell invasion and metastasis-inducing protein 1 (TIAM1) promotes cell migration and invasion in the most common subtype of lung cancer, non-small-cell lung cancer (NSCLC), through an unexpected nuclear function. We show that TIAM1 interacts with TRIM28, a master regulator of gene expression, in the nucleus of NSCLC cells. We reveal that a TIAM1-TRIM28 complex promotes epithelial-to-mesenchymal transition, a phenotypic switch implicated in cell migration and invasion. This occurs through H3K9me3-induced silencing of protocadherins and by decreasing E-cadherin expression, thereby antagonizing cell–cell adhesion. Consistently, TIAM1 or TRIM28 depletion suppresses the migration of NSCLC cells, while migration is restored by the simultaneous depletion of protocadherins. Importantly, high nuclear TIAM1 in clinical specimens is associated with advanced-stage lung adenocarcinoma, decreased patient survival, and inversely correlates with E-cadherin expression.
2023-09-12 | GSE219030 | GEO
Project description:The T lymphoma invasion and metastasis inducing protein 1 (TIAM1) is a guanine nucleotide exchange factor (GEF) that activates the small GTPase RAC1 and regulates a plethora of functions such as cell proliferation, migration, apoptosis and polarity. Recently, we demonstrated that TIAM1 shuttles between the cytoplasm and nucleus. To determine the nuclear role of TIAM1, we performed RNA-seq on SW620 cells transfected either with a specific pre-validated siRNA for TIAM1 (siTIAM1) or a negative control siRNA (siNT) and generated a list of TIAM1 differentially expressed genes. GSEA revealed significant enrichment among TIAM1-regulated genes for YAP-associated molecular signature. To investigate the interplay of TIAM1 with YAP/TAZ we used RNA-seq, generated a list of YAP/TAZ differentially expressed genes from SW620 cells transfected either with specific siRNAs for YAP/TAZ or a negative control siRNA and compared it with the siTIAM1 RNA-seq dataset. Interestingly, we found that 50% of the TAZ/YAP regulated genes were also TIAM1 dependent.
2017-04-26 | GSE90491 | GEO
Project description:We hypothesized that Tiam1 is involved in invassiveness of retinoblastoma. The fuctional role of Tiam1 in cell progression and metastasis was tested by siRNA mediated knockdown of Tiam1 in retinoblastoma Y79 cells. The genes de-regulated in response to Tiam1 knockdown was analysed by cDNA microarray in which most of the actin cytoskeleton regulation proteins and apoptotic proteins were de-regulated. our results prove that Tiam1 modulates actin cytoskeleton and cell invasion in retinoblastoma. Retinoblastoma Y79 cells were treated with Tiam1 siRNA for 48hrs and cDNA microarray was performed to analyze the genes regulated by Tiam1 silencing compared to untreated Y79 cells. Experiments were performed in triplicates.
2013-03-31 | E-GEOD-45130 | biostudies-arrayexpress
Project description:Estrogen Receptor alpha (ERα) is a key driver of most breast cancers, and it is the target of endocrine therapies used in the clinic to treat women with ERα positive (ER+) breast cancer. The two methods ChIP-seq (chromatin immunoprecipitation coupled with deep sequencing) and RIME (Rapid Immunoprecipitation of Endogenous Proteins) have greatly improved our understanding of ERα function during breast cancer progression and in response to anti-estrogens. A critical component of both ChIP-seq and RIME protocols is the antibody that is used to pull down the bait protein. To date, most of the ChIP-seq and RIME experiments for the study of ERα have been performed using the sc-543 antibody from Santa Cruz Biotechnology. However, this antibody has been discontinued, thereby severely impacting the study of ERα in normal physiology as well as diseases such as breast cancer and ovarian cancer. Here, we compare the sc-543 antibody with other commercially available antibodies, and we show that 06-935 (EMD Millipore) and ab3575 (Abcam) antibodies can successfully replace the sc-543 antibody for ChIP-seq and RIME experiments.
2019-03-21 | PXD012930 | Pride
Project description:Rac GTPases are required for neutrophil adhesion and migration, and for the neutrophil effector responses that kill pathogens. These Rac-dependent functions are impaired when neutrophils lack the activators of Rac, Rac-GEFs from the Prex, Vav and Dock families. In this study, we demonstrate that Tiam1 is also expressed in neutrophils, governing focal complexes, actin cytoskeletal dynamics, polarisation and migration, in a manner depending on the integrin ligand to which the cells adhere. Tiam1 is dispensable for the generation of reactive oxygen species but mediates degranulation and NETs release in adherent neutrophils, as well as the killing of bacteria. In vivo, Tiam1 is required for neutrophil recruitment during aseptic peritonitis and for the clearance of Streptococcus pneumoniae during pulmonary infection. However, Tiam1 functions differently to other Rac-GEFs. Instead of promoting neutrophil adhesion to ICAM1 and stimulating β2 integrin activity as could be expected, Tiam1 restricts these processes. In accordance with these paradoxical inhibitory roles, Tiam1 limits the fMLP-stimulated activation of Rac1 and Rac2 in adherent neutrophils, rather than activating Rac as expected. Tiam1 promotes the expression of several regulators of small GTPases and cytoskeletal dynamics, including αPix, Psd4, Rasa3 and Tiam2. It also controls the association of Rasa3, and potentially αPix, Git2, Psd4 and 14‐3‐3ζ/δ, with Rac. We propose these latter roles of Tiam1 underlie its effects on Rac and β2 integrin activity and on cell responses. Hence, Tiam1 is a novel regulator of Rac-dependent neutrophil responses that functions differently to other known neutrophil Rac-GEFs.
2024-01-26 | PXD046791 | Pride
Project description:We hypothesized that Tiam1 is involved in invassiveness of retinoblastoma. The fuctional role of Tiam1 in cell progression and metastasis was tested by siRNA mediated knockdown of Tiam1 in retinoblastoma Y79 cells. The genes de-regulated in response to Tiam1 knockdown was analysed by cDNA microarray in which most of the actin cytoskeleton regulation proteins and apoptotic proteins were de-regulated. our results prove that Tiam1 modulates actin cytoskeleton and cell invasion in retinoblastoma.
2013-03-31 | GSE45130 | GEO