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Identification of genes involved in the cell growth arrest by knockout of BAG3 in human cervical carcinoma HeLa cells

ABSTRACT: BAG3 (BCL2-associated athanogene 3) is a member of the BAG protein family. BAG3 affects a wide variety of cellular events including cell proliferation, apoptosis and autophagy. Recently our data demonstrated that knockout (KO) of BAG3 induces the cell growth arrest in human cervical carcinoma HeLa cells. In the present study, to identify genes involved in the cell growth arrest by BAG3-KO in HeLa cells, global-scale gene expression analysis was carried out using a GeneChip® system.

ORGANISM(S): Homo sapiens

PROVIDER: GSE103475 | GEO | 2017/09/06

SECONDARY ACCESSION(S): PRJNA401788

REPOSITORIES: GEO

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Identification of genes involved in enhancement of hyperthermia sensitivity by knockdown of BAG3 in human oral squamous cell carcinoma cells

Project description:Hyperthermia (HT) treatments in combination with either chemotherapy, radiotherapy or both are used for patients with cancer in various organs. However, the acquisition of thermotolerance in cancer cells due to the increase in cytoprotective proteins attenuates the therapeutic effects of HT. BAG3 (BCL2-associated athanogene 3) is a cytoprotective protein that acts against various stresses including heat stress. Recently, we demonstrated that the inhibition of BAG3 improves cell death sensitivity to HT in cancer cells. However, a detailed molecular mechanism involved in the enhancement of HT sensitivity by BAG3-knockdown (KD) in cancer cells is unclear. In this study, to identify genes involved in the enhancement of HT sensitivity by BAG3-knockdown (KD) in cancer cells, global-scale gene expression analysis was carried out using a GeneChipÂ® system. Human oral squamous carcinoma cell HSC-3 cells were treated with a combination of HT (at 44Â°C for 90 min) and siRNA for BAG3 or luciferase. Total RNA samples were prepared from the cells, and quality of the RNA was analyzed using a Bioanalyzer 2100. Gene expression was analyzed by an Affymetrix GeneChipÂ® system with a Human Genome U133-plus 2.0 array. Sample preparation for array hybridization was carried out as described in the manufacturerâs instructions.

2015-11-19 | E-GEOD-75127 | biostudies-arrayexpress

Identification of genes involved in enhancement of hyperthermia sensitivity by knockdown of BAG3 in human oral squamous cell carcinoma cells

2015-11-19 | GSE75127 | GEO

Overexpression of the human mutation P209L of cochaperone BAG3 in mouse

Project description:An amino acid exchange (P209L) in the HSPB8 binding site of the human cochaperone Bcl2-associated athanogene 3 (BAG3) gives rise to severe dominant childhood cardiomyopathy. To phenocopy the disease in mouse and gain insight into its mechanisms, we have generated humanized transgenic mouse models. Expression of human BAG3P209L-eGFP in mice caused Z-disc disintegration and formation of protein aggregates containing BAG3, components of the Z-disc, and the protein quality control system in cardiomyocytes. This was accompanied by massive fibrosis resulting in a severe, early-onset restrictive cardiomyopathy with increased mortality, as observed in patients. Here we present the shotgun proteome data of mice expressing hBAG3P209L-eGFP compared to control.

2021-04-13 | PXD021165 | Pride

Gene expression profiling of iPSC-derived cardiomyocytes with BAG3 mutations

Project description:Gene expression profiling of wild-type, BAG3-KO and BAG3-R477H iPSC-derived cardiomyocytes

2019-10-10 | GSE138633 | GEO

Bag3-P209L RNA Seq Project

Project description:Cardiac-specific Bag3-P209L transgenic (Tg+) mice develop dilated cardiomyopathy by 12 months of age. The goals of this project are to utilize RNA-sequencing to compare both cardiomyocyte and cardiac fibroblast transcriptomes between aged Bag3-P209L Tg+ and Bag3-WT mice to identify cardiomyocyte and fibroblast specific gene sets that contribute to the functional and morphological changes previously identified in Bag3-P209L Tg+ hearts.

2021-06-25 | GSE116200 | GEO

BAG3 suppresses ciliogenesis by regulating levels of OFD1

Project description:By regulating several hallmarks of cancer, BAG3 exerts oncogenic functions in a wide variety of malignant diseases including glioblastoma (GBM) and triple-negative breast cancer (TNBC). Here we performed global proteomic/phosphoproteomic analyses of Crispr/Cas9-mediated isogenic BAG3 knockouts of the two GBM lines U343 and U251 in comparison to parental controls. Depletion of BAG3 evoked major effects on proteins involved in ciliogenesis/ciliary function and the activity of the related kinases aurora-kinase A (AURKA) and cyclin-dependent kinase-1 (CDK1). Cilia formation was significantly enhanced in BAG3 KO cells, a finding that could be confirmed in BAG3-proficient vs -deficient BT-549 TNBC cells, thus identifying a completely novel function of BAG3 as a negative regulator of ciliogenesis. Furthermore, we demonstrate that enhanced ciliogenesis and reduced expression of SNAI1 and ZEB1, two key transcription factors regulating epithelial to mesenchymal transition (EMT) is correlated to decreased cell migration and invasion, both in the GBM and TNBC BAG3 knockout cells. Our data obtained in two different tumor entities identify suppression of EMT and ciliogenesis as putative synergizing mechanisms of BAG3-driven tumor aggressiveness in therapy-resistant cancers.

2021-06-21 | PXD024802 | Pride

Bag3-P209L RNA Seq Project

Project description:Bag3-P209L RNA Seq Project

| PRJNA477769 | ENA

To characterize bag3 cardiomyopathy model in adult zebrafish through RNA-Seq

Project description:We sequenced mRNA from adult zebrafish heart at 6-month-old bag3 knockout fish and WIK-wildtype controls

2019-08-15 | GSE135823 | GEO

Cytoplasmic proteotoxicity regulates HRI-dependent phosphorylation of eIF2a via the Hsp70-Bag3 module.

Project description:The major heat shock protein Hsp70 has been shown to form a complex with a scaffold protein Bag3, linking it to multiple signaling pathways. Via these interactions, the Hsp70-Bag3 module functions as a proteotoxicity sensor that controls cell signaling. Here, as a tool to identify signaling pathways regulated by this complex, we utilized JG-98, an allosteric inhibitor of Hsp70 that blocks its interaction with Bag3. Gene expression profiling followed by the pathway analysis indicated that a set of signaling pathways including the unfolded protein response (UPR) was activated by JG-98. Surprisingly, only the translation initiation factor eIF2a-associated branch of the UPR was activated under these conditions, while other UPR branches mediating induction of ER chaperones were not induced, suggesting that the response was not related to ER proteotoxicity and thus to ER-associated kinase PERK1. Indeed, induction of the UPR genes under these conditions was dependent on activation of a distinct cytoplasmic eIF2a kinase, HRI. We demonstrated that the Hsp70-Bag3 complex directly interacted with HRI and regulated phosphorylation of eIF2a upon induction of cytoplasmic proteotoxicity. Therefore, we uncovered a novel signaling response, which regulates cell death upon the buildup of abnormal protein species in cytoplasm via an Hsp70-Bag3-HRI-eIF2a axis.

2021-04-14 | GSE171440 | GEO

Phenotypic Screening with Deep Learning Identifies HDAC6 Inhibitors as Cardioprotective Agents in Mouse Models of Dilated Cardiomyopathy

Project description:Dilated cardiomyopathy (DCM) is characterized by reduced cardiac output, as well as thinning and enlargement of left ventricular chambers. These characteristics eventually lead to heart failure. Current standards of care do not target the underlying molecular mechanisms associated with genetic forms of heart failure, driving a need to develop novel therapeutics for DCM. To identify candidate therapeutics, we developed an in vitro DCM model using induced pluripotent stem cell–derived cardiomyocytes (iPSC-CMs) deficient in BCL2-associated athanogene 3 (BAG3). With these BAG3-deficient iPSC-CMs, we identified cardioprotective drugs with a phenotypic screen and deep learning. Using a library of 5500 bioactive compounds and siRNA validation, we identified that inhibiting histone deacetylase 6 (HDAC6) was cardioprotective at the sarcomere level. We translated this finding to a BAG3 cardiac-knockout (BAG3cKO) mouse model of DCM, showing that inhibiting HDAC6 with two isoform-selective inhibitors (tubastatin A and a novel inhibitor TYA-018) protected heart function. In BAG3cKO and BAG3 E455K mice, HDAC6 inhibitors improved left ventricular ejection fraction and reduced left ventricular diameter at diastole and systole. We also found that HDAC6 inhibitors protected the microtubule network from mechanical damage, increased autophagic flux, decreased apoptosis, and reduced inflammation in the heart. Our results demonstrate the power of combining iPSC-CMs with phenotypic screening and deep learning to accelerate target and drug discovery, and they support the development of novel therapies that address underlying mechanisms associated with heart disease.

2021-12-31 | GSE179656 | GEO

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