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RNA-seq of METTL3 knockdown in prostate cancer cells

ABSTRACT: RNA-seq of METTL3 knockdown in prostate cancer cells

PROVIDER: PRJNA1004597 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25618296_1.fastq.gz	Fastqsanger.gz
	SRR25618296_2.fastq.gz	Fastqsanger.gz
	SRR25618297_1.fastq.gz	Fastqsanger.gz
	SRR25618297_2.fastq.gz	Fastqsanger.gz
	SRR25618298_1.fastq.gz	Fastqsanger.gz

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RNA-seq of METTL3 knockdown in prostate cancer cells

Project description:Prostate cancer (PCa) is the most frequently diagnosed malignancy in men worldwide. METTL3 play nonnegligible function in PCa progression. Here, we seek to explore the effect of METTL3 on transcriptome profile in PC3 cells via RNA-seq.

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Mapping of m6A and Its Regulatory Targets in Prostate Cancer Reveals a METTL3-low Induction of Therapy Resistance

Project description:Genomic and transcriptomic alterations are insufficient to explain the variance in protein expression seen in cancer. Recent evidence has highlighted the role of N6-methyladenosine (m6A) in the regulation of mRNA expression, stability and translation, supporting a potential role for post-transcriptional regulation mediated by m6A in cancer. Here we explore prostate cancer as an exemplar cancer and generate the first prostate m6A maps, and further examined how low levels of N6-adenosine-methyltransferase (METTL3) associates with advanced prostate cancer and results in altered expression at the level of transcription, translation, and protein. In particular extracellular matrix proteins have a high number of m6A sites and show significant changes in expression with METTL3 knock-down. We also discovered the upregulation of a hepatocyte nuclear factor-driven gene signature that is associated with therapy resistance in prostate cancer. Significantly, METTL3 knock-down rendered the cells resistant to androgen receptor antagonists, implicating changes in m6A as a mechanism for therapy resistance in metastatic prostate cancer.

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METTL3 promotes translation in human cancer cells

Project description:we find METTL3 associates with polyribosomes and promotes translation. METTL3 depletion inhibits translation, and both wild-type and catalytically inactive METTL3 promote translation when tethered to the 3' untranslated region (UTR) of a reporter mRNA. Mechanistically, METTL3 enhances mRNA translation through an interaction with the translation initiation machinery. m6A seq in A549 and H1299 cells, RNA seq in METTL3 knockdown cells

2016-07-03 | E-GEOD-76367 | biostudies-arrayexpress

The METTL3 RNA methyltransferase regulates gene expression in castrate resistant LNCaP:C42 prostate cancer cells

Project description:RNA sequencing was used to determine the effect of the STM2457 METTL3 inhibitor on prostate cancer cell gene expression.

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RNA-seq of human breast cancer cell lines with METTL3 knockdown

Project description:We assess the effect of METTL3 on gene expression and transcriptional splicing in three different human breast cancer cell lines

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Chromatin-occupancy profiling of PRMT5 and METTL3 in prostate cancer cells

Project description:Prostate cancer (PCa) is the most frequently diagnosed malignancy in men worldwide. Epigenetic regulation has been recognized as a main mechanism of cancer evolution. PRMT5 is the major type II protein arginine methyltransferase catalyzing the symmetric dimethylation of arginine, and METTL3 is the enzymatic component of the large N6-adenosine-methyltransferase complex in mammalian responsible for N6-methyladenosine (m6A) modification in diverse RNA species. Both genes are found upregulated in PCa. However, their exact functional contribution to prostate tumorigenesis is unknown. As both proteins can regulate transcription via binding to chromatin, we seek to explore their DNA binding profiles in both AR+ LNCaP and AR- PC3 cells via recently developed CUT&Tag technique. Antibodies we used were Active Motif #61001 for PRMT5 and Abcam #195352 for METTL3. Our data suggests that both proteins regulate PCa cell biology, at least partially, through chromatin-binding and subsequent transcriptional regulation. CUT&Tag assay for arginine methyltransferase PRMT5 and N6‐adenosine‐methyltransferase METTL3 in LNCaP and PC3 cells

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Effect of METTL3 knockdown on MCF10 breast cancer progression model

Project description:To investigate the cellular role of METTL3 in breast cancer progression, we established MCF10-A, MCF10-AT1, and MCF10-CA1H cell lines that had knockdown of METTL3 using CRISPR. We then performed gene expression profiling analysis using data obtained from RNA-seq of the various cell lines.

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Project description:To identify changes in splicing patterns following METTL3 knockdown, RNA-sequencing was performed on nuclear RNA extracted from cells transfected with METTL3-targeting siRNA or a non-targeting siRNA (siControl).

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