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A TGFbeta-PRMT5-MEP50 Axis Regulates Cancer Cell Invasion through Histone H3 and H4 Arginine Methylation Coupled Transcriptional Activation and Repression

ABSTRACT: We sequenced mRNA from 3 biological replicates each of A549 lung adenocarcinoma cell lines expressing shRNA against GFP (control), PRMT5, or MEP50. We then determined differential gene expression. Transcriptome analysis of mRNA testing the role of PRMT5 and MEP50 by knockdown in A549 human lung adenocarcinoma cells

ORGANISM(S): Homo sapiens

SUBMITTER: David Shechter

PROVIDER: E-GEOD-80182 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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A TGFβ-PRMT5-MEP50 axis regulates cancer cell invasion through histone H3 and H4 arginine methylation coupled transcriptional activation and repression.

Chen H H Lorton B B Gupta V V Shechter D D

Oncogene 20160606 3

Protein arginine methyltransferase 5 (PRMT5) complexed with MEP50/WDR77 catalyzes arginine methylation on histones and other proteins. PRMT5-MEP50 activity is elevated in cancer cells and its expression is highly correlated with poor prognosis in many human tumors. We demonstrate that PRMT5-MEP50 is essential for transcriptional regulation promoting cancer cell invasive phenotypes in lung adenocarcinoma, lung squamous cell carcinoma and breast carcinoma cancer cells. RNA-Seq transcriptome analys ...[more]

PMID: 27270440

Similar Datasets

A TGFbeta-PRMT5-MEP50 Axis Regulates Cancer Cell Invasion through Histone H3 and H4 Arginine Methylation Coupled Transcriptional Activation and Repression

Project description:We sequenced mRNA from 3 biological replicates each of A549 lung adenocarcinoma cell lines expressing shRNA against GFP (control), PRMT5, or MEP50. We then determined differential gene expression.

2016-06-09 | GSE80182 | GEO

PRMT5 inhibition increases PD-L1 expression and immunoresistance in lung cancer

Project description:Purpose: We sequenced mRNA from 3 biological replicates each of NCI-H460 lung adenocarcinoma cell lines expressing shRNA against GFP (control) or PRMT5.We then determined differential gene expression to identify the relationship between PRMT5 expression and tumorigenesis. Methods: PRMT5 shRNA and control shRNA NCI-H460 cells were generated by lentivirus targeting PRMT5 or GFP(control), in triplicate,using illumina Novaseq™ 6000. Results:PRMT5 specific knockdown cells were enriched in the negative regulation of T cells and type I IFN response,we found that negative regulation of T cell molecules like Arg2, CD274 and IDO1 were increased in the PRMT5 shRNA group compared with the control group.

2022-02-08 | GSE178521 | GEO

Genome-wide analysis of genes regulated by p44/wdr77 and PRMT5 in lung and prostate cancer cells

Project description:Analysis of gene expression in lung and prostate cancer cells expressing non-target (NT), p44/wdr77. or PRMT5 shRNA. Results provide important information on how p44/wdr77 and PRMT5 control cellular proliferation. Total RNA obtained from cells expressing NT, p44/wdr77, or PRMT5 shRNA.

2014-04-14 | E-GEOD-56757 | biostudies-arrayexpress

Glutathionylation decreases methyltransferase activity of PRMT5 and inhibits cell proliferation

Project description:Glutathionylation is an important posttranslational modification that protects proteins from further oxidative damage as well as influencing protein structure and activity. In the present study, we demonstrate that the cysteine-42 residue in protein arginine N-methyltransferase 5 (PRMT5) is glutathionylated in aged mice or in cells that have been exposed to oxidative stress. Deglutathionylation of this protein is catalyzed by glutaredoxin-1 (Grx1). Using mutagenesis and subsequent biochemical analyses, we show that glutathionylation decreased the binding affinity of PRMT5 with methylosome protein-50 (MEP50) and reduced the methyltransferase activity of PRMT5. Furthermore, overexpression of PRMT5-C42A mutant caused a significant increase in histone methylation in HEK293T and A549 cells and promoted cell growth, whereas overexpression of the PRMT5-C42D mutant, a mimic of glutathionylated PRMT5, inhibited cell proliferation. Taken together, our results demonstrate a new mechanism of regulation of PRMT5 methyltransferases activity and suggest that PRMT5 glutathionylation is partly responsible for reactive oxygen species-mediated cell growth inhibition

2020-09-02 | PXD020428 | Pride

Total RNA-seq in the A549 cell line after glucocorticoid re-induction

Project description:We performed total RNA-seq in the A549 cell line. Cells were treated with either 100 nM dexamethasone or 0.1% ethanol. After 4 hours, cells were washed 2x with PBS and cultured in hormone-free medium for 24 hours, after which cells were treated again for 4 hours with either 100 nM dexamethasone or 0.1% ethanol.

2021-05-03 | E-MTAB-9923 | biostudies-arrayexpress

PRMT5 is essential for sustaining normal adlut hematopoiesis

Project description:Examining the effects of PRMT5 loss on the gene expression profile of hematopoietic stem and progenitor cells We established the PRMT5 conditional KO mice, and bred the mice with Mx1 cre transgenic mice to delete PRMT5 in hematopoietic cells. We isolated hematopoetic stem and progenitor cells 3 days after PRMT5 deletion, and examined the gene expression files using RNA-sequencing.

2015-07-15 | E-GEOD-69937 | biostudies-arrayexpress

SOX2 gene regulates the transcriptional network of oncogenes and affects tumorigenesis of human lung cancer cells

Project description:Recent studies demonstrated that cancer stem cells (CSCs) have higher tumorigenesis properties than those of differentiated cancer cells and that transcriptional factor-SOX2 plays a vital role in maintaining the unique properties of CSCs; however, the function and underlying mechanism of SOX2 in carcinogenesis of lung cancer are still elusive. This study applied immunohistochemistry to analyze the expression of SOX2 in human lung tissues of normal individuals as well as patients with adenocarcinoma, squamous cell carcinoma, large cell and small cell carcinoma and demonstrated specific overexpression of SOX2 in all types of lung cancer tissues. This finding supports the notion that SOX2 contributes to the tumorigenesis of lung cancer cells and can be used as a diagnostic probe. In addition, obviously higher expression of oncogenes c-MYC, WNT1, WNT2 and NOTCH1 was detected in side population (SP) cells than in none side population (NSP) cells of human lung adenocarcinoma cell line-A549, revealing a possible mechanism for the tenacious tumorigenic potential of CSCs. To further elucidate the function of SOX2 in tumorigenesis of cancer cells, A549 cells were established with expression of luciferase and doxycycline inducible shRNA targeting SOX2. We found silencing of SOX2 gene reduces the tumorigenic property of A549 cells with attenuated expression of c-MYC, WNT1, WNT2 and NOTCH1 in xenografted NOD/SCID mice. By RNA-Seq method, additional 246 target cancer genes of SOX2 were revealed. These results present evidence that SOX2 may regulate the expression of oncogenes in CSCs to promote the development of human lung cancer. Examination of mRNA profiles in A549 cells with SOX2 silencing

2012-08-31 | E-GEOD-36597 | biostudies-arrayexpress

Effect of Prmt5 deletion on Dermo1 gene expression in lung mesenchymal cells of C57 mice at E18.5.

Project description:To investigate the role of Prmt5 gene in lung development, we established a Prmt5 specific knockout model in Dermo1 of C57 mouse lung mesenchymal cells using cre-loxp system. Then, the data obtained from RNA-seq in E18.5-day lung tissues were used for gene expression profiling analysis.

2023-10-31 | GSE215805 | GEO

MRTX1719 is an MTA-cooperative PRMT5 inhibitor that exhibits synthetic lethality in preclinical models and patients with MTAP deleted cancer

Project description:Previous studies implicated PRMT5 as a synthetic lethal target for MTAP deleted (MTAP del) cancers, however, the pharmacological characterization of small molecule inhibitors that recapitulate the synthetic lethal phenotype have not been described. MRTX1719 selectively inhibited PRMT5 in the presence of MTA, which is elevated in MTAP del cancers, and inhibited PRMT5-dependent activity and cell viability with >70-fold selectivity in HCT116 MTAP del compared to HCT116 MTAP WT cells. MRTX1719 demonstrated dose-dependent anti-tumor activity and inhibition of PRMT5-dependent SDMA modification in MTAP del tumors. In contrast, MRTX1719 demonstrated minimal effects on SDMA and viability in MTAP WT tumor xenografts, mouse or human hematopoietic cells. MRTX1719 demonstrated marked anti-tumor activity across a panel of xenograft models at well-tolerated doses. Early signs of clinical activity were observed including objective responses in patients with MTAP del melanoma, gallbladder adenocarcinoma, mesothelioma, non-small cell lung cancer, and MPNST from the Phase 1/2 study. Significance: PRMT5 was identified as a synthetic lethal target for MTAP del cancers, however, previous PRMT5 inhibitors do not selectively target this genotype. The differentiated binding mode of MRTX1719 leverages the elevated MTA in MTAP del cancers and represents a promising therapy for the ~10% of cancer patients with this biomarker.

2023-08-09 | GSE240145 | GEO

Histone arginine methylation by Prmt5 is required for lung branching morphogenesis through repression of BMP signaling

Project description:Branching morphogenesis is essential for the successful development of a functional lung to accomplish its gas exchange function. Although many studies have highlighted requirements for the bone morphogenetic protein (BMP) signaling pathway during branching morphogenesis, little is known about how BMP signalingis regulated. Here we report that the protein arginine methyltransferase 5 (Prmt5) and symmetric dimethylation at histone H4 arginine 3 (H4R3sme2) directly associate with chromatin of Bmp4 to suppress its transcription. Inactivation of Prmt5 in the lung epithelium results in halted branching morphogenesis, altered epithelial cell differentiation and neonatal lethality. These defects are accompanied by increased apoptosis and reduced proliferation of lung epithelium, as a consequence of elevated canonical BMP-Smad1/5/9 signaling. Inhibition of BMP signaling by Noggin rescues the lung branching defects of Prmt5 mutant in vitro. Taken together, our results identify a novel mechanism through which Prmt5-mediated histone arginine methylation represses canonical BMP signaling to regulate lung branching morphogenesis.

2024-05-23 | GSE229423 | GEO

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