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RNA-seq of malignant pleural mesothelioma cell line MSTO-211H upon silencing of lncRNA linc00941

ABSTRACT: RNA-seq of malignant pleural mesothelioma cell line MSTO-211H upon silencing of lncRNA linc00941

PROVIDER: PRJEB67293 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR12095774_1.fastq.gz	Fastqsanger.gz
	ERR12095774_2.fastq.gz	Fastqsanger.gz
	ERR12095775_1.fastq.gz	Fastqsanger.gz
	ERR12095775_2.fastq.gz	Fastqsanger.gz
	ERR12095776_1.fastq.gz	Fastqsanger.gz

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RNA-seq of malignant pleural mesothelioma cell line MSTO-211H upon silencing of lncRNA linc00941

Project description:Identification of transcriptional program influenced by the expression of lncRNA linc00941 in malignant pleural mesothelioma cell line MSTO-211H. Linc00941 expression was knocked-down through siRNA strategy.

2024-09-30 | E-MTAB-13400 | biostudies-arrayexpress

Pharmacodynamics of malignant mesothelioma MSTO-211H dn-TEAD2 xenograft recurrence.

Project description:Pharmacodynamics of malignant mesothelioma MSTO-211H dn-TEAD2 xenograft recurrence.

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TRIM28 controls the expression of the G2/M gene program and is required for mitosis execution in malignant pleural mesothelioma.

Project description:The goal of this experiment was to get deep into TRIM28 biological function in malignant pleural mesothelioma. To this end MSTO-211H cell line was infected by two different sgRNAs targeting TRIM28 and a non-targeting sgRNA as control. Two independent experiments were performed.RNA was collected 7 days after infection and changes in gene expression were analyzed by mRNA-seq.

2023-09-16 | E-MTAB-10942 | biostudies-arrayexpress

Pharmacodynamics of malignant mesothelioma MSTO-211H dn-TEAD2 xenograft recurrence.

Project description:We investigate the dependence of human malignant pleural mesothelioma on a functional YAP1-TEAD transcription factor complex to maintain fully established tumors in vivo. We show that, in a dysfunctional Hippo genetic background, expression of a doxycycline-dependent dominant negative TEAD2 temporarily modulates YAP1/TEAD-dependent gene expression and inhibits growth of established tumor xenografts. Recovery of tumor growth is associated with TEAD-dependent transcription comparable to untreated tumors, therefore, re-activation of TEAD transcription complexes.

2022-02-17 | GSE196714 | GEO

Combined dopamine receptor inhibition and radiotherapy target mesothelioma-initiating cells and increase survival in a mouse model of mesothelioma

Project description:Malignant pleural mesothelioma (MPM) is a rare thoracic cancer associated with poor prognosis and low survival rates. In solid cancers, repurposed dopamine receptor antagonists have been shown to have anti-cancer effects. Moreover, in combination with radiotherapy, quetiapine (QTP), a dopamine (D) 2/3 receptor antagonist, has been shown to interfere with self-renewal capacity in glioma-initiating cells and increase survival in mouse models of glioblastoma. In this study we explore combined treatment effects in MPM. Using mesothelioma cell lines, MSTO-211H, H2052, and H2452, and MSTO-211H-derived orthotopic xenograft mouse model of MPM we examined how QTP combined with radiation affects mesothelioma-initiating cells (MICs) in vitro and survival in vivo. Subsequently, bulk and single cell RNA sequencing was used to characterize the transcriptomic landscape of MSTO-211H treated with combined radiation and QTP. We demonstrate that combining QTP with radiation reduces MIC self-renewal capacity and stem cell frequency. In vivo, this combination therapy significantly extends the median survival of mesothelioma-bearing mice. Clonogenic survival assays revealed that QTP does not enhance radiosensitivity in the tested mesothelioma cell lines. Sequencing data revealed, combined treatment upregulated genes involved in cholesterol homeostasis, depleted cancer stem cells, and increased cellular senescence. Taken together, our study highlights the therapeutic potential of radiation with QTP in the treatment of MPM.

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Combined dopamine receptor inhibition and radiotherapy target mesothelioma-initiating cells and increase survival in a mouse model of mesothelioma [scRNA-Seq]

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Deoxypodophyllotoxin suppresses Malignant pleural mesothelioma growth via mitotic dependent necroptosis

Project description:Malignant pleural mesothelioma (MPM) is a highly aggressive tumor with a poor prognosis. Patients are typically diagnosed at an advanced stage due to the disease's long incubation period. Limited therapeutic advancements in the last two decades have prompted further investigation into alternative treatments. Previous studies have identified significant dysregulation in the mitotic spindle assembly checkpoint pathway and microtubule network of MPM, underscoring the potential of targeting microtubules in managing MPM. Deoxypodophyllotoxin (DPT) is a novel microtubule-targeting drug that has demonstrated promising therapeutic efficacy in various cancers. While the precise mechanism of DPT's anti-MPM effect remains undisclosed, our research indicates that DPT inhibits MPM growth in a dose-dependent manner both in vitro and in vivo. Moreover, it exhibits a favorable safety profile and shows lower toxicity towards normal cells and mice at therapeutic doses. Mechanistic studies involving three MPM cell lines (MSTO-211H, H2452, and H28) revealed that DPT induces multinucleated and micronucleated cells, disrupts spindle formation, and triggers Mitosis cell cycle arrest and necroptosis in tumor cells. In conclusion, our findings suggest that DPT holds promise as a safe and effective therapeutic option for MPM.

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Conditional expression of sh-YAP1 modulates YAP1/TEAD-dependent transcription and causes regression of established human malignant mesothelioma MSTO-211H [sh-YAP1] xenografts.

Project description:We investigate the dependence of human malignant pleural mesothelioma on a functional YAP1-TEAD transcription factor complex to maintain fully established tumors in vivo. We show that, in a dysfunctional Hippo genetic background, downregulation of YAP1 by shRNA results in modulation of YAP1/TEAD-dependent gene expression and regression of established tumor xenografts. Our data demonstrate that, in the context of a mutated Hippo pathway, YAP1 activity is essential to maintain the growth of mesothelioma cells in vivo, thus validating the concept of inhibiting the activated YAP1/TEAD complex for the treatment of malignant pleural mesothelioma patients.

2022-02-17 | GSE196672 | GEO

Conditional expression of a dominant negative-TEAD2 construct modulates YAP1/TEAD-dependent transcription and arrests growth of human malignant mesothelioma MSTO-211H [TEAD2-dn] xenografts.

Project description:We investigate the dependence of human malignant pleural mesothelioma on a functional YAP1-TEAD transcription factor complex to maintain fully established tumors in vivo. We show that, in a dysfunctional Hippo genetic background, expression of a dominant negative TEAD2 modulates YAP1/TEAD-dependent gene expression and inhibits growth of established tumor xenografts. Our data demonstrate that, in the context of a mutated Hippo pathway, TEAD2 activity is essential to maintain the growth of mesothelioma tumors in vivo, thus validating the concept of inhibiting the activated YAP1/TEAD complex for the treatment of malignant pleural mesothelioma patients.

2022-02-17 | GSE196691 | GEO

Immunopeptidomics of malignant mesothelioma to identify target antigens for T cell Immunotherapy

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

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