IKK in mesothelioma
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA533336 | ENA |
REPOSITORIES: ENA
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Project description:perform gene expression silencing for both IKKs in AE17, AB2 and KPM1 cells using lentiviral shRNA pools. After validating gene silencing, RNA was extracted from both parental (shC) and daughter cells (shChuk, shIkbkb) and was send for RNAsequencing in order to define possible target genes, up or down regulated upon gene expression manipulation with lentiviral shRNA. These cell lines (parental and daughter) were evaluated in vitro for the role of IKKs in cell proliferation, survival and clonogenicity and in vivo for their impact in MPM development upon intrapleural injection in mice
2025-04-05 | GSE129984 | GEO
Project description:Desmoplastic malignant mesothelioma is a rare tumor. Due to the rarity, genomic profile of desmoplastic malignant mesothelioma is not unveiled. To elucidate genomic profile of desmoplastic malignant mesothelioma, we used illumina infinium omini exomeexpress in an established patient-derived cell line of desmoplastic malignant mesothelioma.
2021-10-18 | GSE185549 | GEO
Project description:Genomic characterization of mesothelioma patients by CGH arrays. Genomic characterization of mesothelioma patients by CGH arrays.
2018-04-01 | GSE67487 | GEO
Project description:RIPK3 locus is methylated in mesothelioma cell lines
2021-02-24 | GSE158768 | GEO
Project description:The 5' AMP-activated protein kinase (AMPK) is a master energy sensing kinase that is regulated by phosphorylation of Thr172 in its activation loop. Three kinases can phosphorylate AMPK at Thr172: the tumor suppressor LKB1, CAMKK2 and TAK1. While LKB1- and CAMKK2-mediated AMPK Thr172 phosphorylation have been well-characterized, much less is known about TAK1-dependent AMPK phosphorylation. An important target of TAK1 is IκB kinase (IKK) which controls NF-B transcription factor activation. Here, we tested the hypothesis that IKK acted downstream of TAK1 to activate AMPK by phosphorylating Thr172. IKK was required for phosphorylation of Thr172 in AMPK in response to treatment with IL-1 or TNF- treatment or by TAK1 overexpression. Additionally, IKK regulated basal AMPK Thr172 phosphorylation in several cancer cell types independently of TAK1, indicating that other modes of IKK activation could lead to AMPK activation. We found that IKK directly phosphorylated AMPK at Thr172 independently of LKB1 or energy stress. This finding indicated that while LKB1 activates AMPK as a sensor of energetic stress, IKK activated AMPK in response to extracellular inflammatory signals and through distinct pathways downstream of IKK activation. Accordingly, in LKB1-deficient cells, IKK inhibition caused a reduction in AMPK Thr172 phosphorylation in response to the mitochondrial inhibitor phenformin. This response led to enhanced apoptosis and suggests that IKK inhibition in combination with phenformin could be used clinically to treat patients with LKB1-deficient cancers.
2018-07-16 | PXD009897 | Pride
Project description:Immunoaffinity purification was performed on human mesothelioma cell lines NCI-H2452, NCI-H28, MSTO-211H and JL1, on murine mesothelioma cell line AB12, as well as on mesothelioma samples from two patients (including tumor and benign tissues). Thereafter Immunopeptidomics by Mass Spectrometry on a Tims TOF Pro revealed the MHC peptide landscape of mesothelioma.
2023-09-08 | PXD038273 | Pride
Project description:Malignant Peritoneal Mesothelioma (PeM) is a rare but frequently fatal cancer that originates from the peritoneal lining of the abdomen. Standard treatment of PeM is limited to cytoreductive surgery and/or chemotherapy, and no targeted therapies for PeM yet exist. This study performs comprehensive integrative analysis of genome, transcriptome, and proteome of treatment-naïve PeM tumors with the aim of identifying mesothelioma-related molecular alterations and potentially identifying novel treatment strategies.
2018-12-11 | PXD008873 | Pride
Project description:Desmoplastic malignant mesothelioma is a rare tumor. Due to the rarity, development of new treatment for desmoplastic malignant mesothelioma is difficult. To develop new treatment strategy using existing anti-cancer drugs, kinase activity profiling has not been thoroughly studied. We used PamChip array to identify the peptide profiles of desmoplastic malignant mesothelioma between the patient-derived cell line and the tumor tissue.
2021-10-01 | GSE185107 | GEO
Project description:Mesothelioma is an aggressive cancer of the mesothelial layer associated with an extensive fibrotic response. The latter is in large part mediated by cancer-associated fibroblasts which mediate tumour progression and poor prognosis. However, understanding of the crosstalk between cancer cells and fibroblasts in this disease is mostly lacking. Here, using co-cultures of patient-derived mesothelioma cell lines and lung fibroblasts, we demonstrate that fibroblast activation is a self-propagated process producing a fibrotic extracellular matrix (ECM) and triggering drug resistance in mesothelioma cells. Following characterisation of mesothelioma cells/fibroblasts signalling crosstalk, we identify several FDA-approved targeted therapies as far more potent than standard-of-care Cisplatin/Pemetrexed in ECM-embedded co-culture spheroid models. In particular, the SRC family kinase inhibitor, Saracatinib, extends overall survival well beyond standard-of-care in a mesothelioma genetically-engineered mouse model. In short, we lay the foundation for the rational design of novel therapeutic strategies targeting mesothelioma/fibroblast communication for the treatment of mesothelioma patients.
2024-01-26 | PXD040492 | Pride
Project description:Background: Malignant mesothelioma is an aggressive cancer with poor prognosis. It is characterized by prominent extracellular matrix, mesenchymal tumor cell phenotypes and chemoresistance. In this study, the ability of pirfenidone to alter mesothelioma cell proliferation and migration as well as mesothelioma tumor microenvironment was evaluated. Pirfenidone is an anti-fibrotic drug used in the treatment of idiopathic pulmonary fibrosis and has also anti-proliferative activities. Aims: Transcriptional profiling using RNA sequencing of human mesothelioma xenograft tumors treated with PBS or pirfenidone. Aim was to compare extracellular matrix and fibrosis related genes. Results: Treatment of mice harboring mesothelioma xenografts with pirfenidone alone did not reduce tumor proliferation in vivo. However, pirfenidone modified the tumor microenvironment by reducing the expression of extracellular matrix associated genes. In addition, GREM1 expression was downregulated by pirfenidone in vivo. Conclusion: By reducing two major upregulated pathways in mesothelioma and by targeting tumor cells and the microenvironment pirfenidone may present a novel anti-fibrotic and anti-cancer adjuvant therapy for mesothelioma.
2018-12-14 | GSE113803 | GEO