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A novel therapeutic strategy targeting the mesenchymal phenotype of malignant pleural mesothelioma by suppressing LSD1

ABSTRACT: A novel therapeutic strategy targeting the mesenchymal phenotype of malignant pleural mesothelioma by suppressing LSD1

PROVIDER: PRJNA754799 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15464294_1.fastq.gz	Fastqsanger.gz
	SRR15464294_2.fastq.gz	Fastqsanger.gz
	SRR15464295_1.fastq.gz	Fastqsanger.gz
	SRR15464295_2.fastq.gz	Fastqsanger.gz
	SRR15464296_1.fastq.gz	Fastqsanger.gz

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A novel therapeutic strategy targeting the mesenchymal phenotype of malignant pleural mesothelioma by suppressing LSD1 [array]

Project description:Transcriptome analysis following knock down of LSD1 in ACC-MESO-1 cells. Malignant pleural mesothelioma (MPM) is a highly aggressive tumor that has a low overall survival; however, no significant treatment advances have been made in the past 15 years. In this study we investigated whether targeting lysine-specific demethylase 1 (LSD1/KDM1), a histone-modifying enzyme responsible for demethylating histone H3 lysine 4 and lysine 9, could represent a novel therapeutic strategy for patients with MPM. We found that suppressing LSD1 induces an epithelial phenotype in sarcomatoid MPM cells, while attenuating the mesenchymal phenotype sensitized MPM cells to cisplatin-induced apoptosis through the FAK pathway. To investigate the potential mechanisms underlying FAK pathway activation, we performed transcriptome analysis using two different shRNA constructs against the LSD1.

2021-08-10 | GSE181735 | GEO

A novel therapeutic strategy targeting the mesenchymal phenotype of malignant pleural mesothelioma by suppressing LSD1 [array]

Project description:A novel therapeutic strategy targeting the mesenchymal phenotype of malignant pleural mesothelioma by suppressing LSD1 [array]

| PRJNA753128 | ENA

A novel therapeutic strategy targeting the mesenchymal phenotype of malignant pleural mesothelioma by suppressing LSD1 [ATAC-seq]

Project description:A novel therapeutic strategy targeting the mesenchymal phenotype of malignant pleural mesothelioma by suppressing LSD1 [ATAC-seq]

| PRJNA754805 | ENA

A novel therapeutic strategy targeting the mesenchymal phenotype of malignant pleural mesothelioma by suppressing LSD1 [ATAC-seq]

Project description:ATAC-seq analysis of following knock down of LSD1 in ACC-MESO-1 cells.

2021-08-16 | GSE182153 | GEO

Identification of novel markers for malignant pleural mesothelioma diagnosis

Project description:Diagnosis of malignant pleural mesothelioma (MPM) is difficult, the most common differential diagnosis being benign pleural diseases and metastatic adenocarcinomas. In order to identify novel markers able to improve diagnostic accuracy, we performed a genome-wide gene expression analysis on tumor cells lines established from pleural effusions (13 MPM and 4 lung adenocarcinoma). Our microarray analysis led to the identification of genes encoding novel cellular and soluble markers whose expression was validated by RT-qPCR. Immunohistochemical staining of tumor biopsies with anti-type-III collagen antibodies were positive in mesothelioma cells but not in adenocarcinoma cells. Using ELISA, we showed that the C-C motif chemokine 2 (CCL2) concentration was significantly higher in pleural effusions from patients with mesothelioma (n = 61) than in subjects with adenocarcinoma (n = 25) or with benign pleural effusions (n = 15): median (interquartile range) = 2.99 ng/mL (1.76-6.01) versus 0.99 ng/mL (0.51-1.83) and 1.47 ng/mL (0.80-1.56), respectively, P < 0.0001. Conversely, the galectin-3 concentration was lower in mesothelioma: 11.50 ng/mL (6.73-23.53) versus 24.74 ng/mL (20.42-70.35) and 17.64 ng/mL (14.81-24.68), respectively, P < 0.0001. The AUC for CCL2 were 0.8030 and 0.7716 for differentiating mesothelioma from adenocarcinoma or benign effusions, respectively. Similarly, the AUC obtained for galectin-3 were 0.7980 and 0.6923, respectively. In conclusion, type-III collagen, CCL2 and galectin-3 are promising new diagnostic markers for mesothelioma.

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