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Effect of silencing of METTL1 oncastration-resistant prostate cancer cells

ABSTRACT: Effect of silencing of METTL1 oncastration-resistant prostate cancer cells

PROVIDER: PRJNA1000936 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25475136_1.fastq.gz	Fastqsanger.gz
	SRR25475136_2.fastq.gz	Fastqsanger.gz
	SRR25475137_1.fastq.gz	Fastqsanger.gz
	SRR25475137_2.fastq.gz	Fastqsanger.gz
	SRR25475138_1.fastq.gz	Fastqsanger.gz

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Effect of silencing of METTL1 on gene expression of castration-resistant prostate cancer cells LNCaP-AI via RNA-seq technology.

Project description:Background: N7-methylguanosine (m7G) modification is, a more common epigenetic modification in addition to m6A modification, mainly found in mRNA capsids, mRNA interiors, transfer RNA (tRNA), pri-miRNA, and ribosomal RNA (rRNA). It has been found that m7G modifications play an important role in mRNA transcription, tRNA stability, rRNA processing maturation, and miRNA biosynthesis. However, the role of m7G modifications within mRNA and its “writer” methyltransferase 1(METTL1) in tumors, particularly prostate cancer (PCa), has not been revealed. Methods： The differential expression level of METTL1 between hormone-sensitive prostate cancer (HSPC) and castrate-resistant prostate cancer (CRPC) was evaluated via RNA-seq and in vitro experiments. The effects of METTL1 on CRPC progression were investigated through in vitro and in vivo assays. The upstream molecular mechanism of METTL1 expression upregulation and the downstream mechanism of its action were explored via Chromatin Immunoprecipitation quantitative reverse transcription polymerase chain reaction (CHIP-qPCR), Co-immunoprecipitation (Co-IP), luciferase reporter assay, transcriptome-sequencing, m7G AlkAniline-Seq, and mRNA degradation experiments, etc. Results and conclusion： Here, we found that METTL1 was elevated in CRPC and that patients with METTL1 elevation tended to have a poor prognosis. Functionally, the knockdown of METTL1 in CRPC cells significantly limited cell proliferation and invasive capacity. Mechanistically, we unveiled that P300 can form a complex with SP1 and bind to the promoter region of the METTL1 gene via SP1, thereby mediating METTL1 transcriptional upregulation in CRPC. Subsequently, our findings indicated that METTL1 leads to enhanced mRNA stability of CDK14 by adding m7G modifications inside its mRNA, ultimately promoting CRPC progression.

2023-08-22 | GSE239768 | GEO

Effect of silencing of METTL1 on m7G modification within mRNA of castration-resistant prostate cancer cells LNCaP-AI via m7G AlkAniline-Seq analysis. [m7G]

2023-08-22 | GSE239766 | GEO

Effect of silencing of METTL1 on gene expression of castration-resistant prostate cancer cells LNCaP-AI via RNA-seq technology.

Project description:Effect of silencing of METTL1 on gene expression of castration-resistant prostate cancer cells LNCaP-AI via RNA-seq technology.

| PRJNA1000941 | ENA

METTL1 promotes tumorigenesis through tRNA-derived fragment biogenesis in prostate cancer

Project description:Newly growing evidence highlights the essential role that epitranscriptomic marks play in the development of cancer; however, little is known about the role and implications of altered epitranscriptome deposition in prostate cancer. Here, we show that the transfer RNA N7-methylguanosine (m7G) transferase METTL1 is highly expressed in primary and advanced prostate tumours. Mechanistically, we find that METTL1 depletion causes the loss of m7G tRNA methylation and promotes the biogenesis of a novel class of small non-coding RNAs derived from 5’tRNA fragments. 5′ tRNA-derived small RNAs steer translation control to favour the synthesis of key regulators of tumour growth suppression, interferon pathway, and immune effectors. Knockdown of Mettl1 in prostate cancer preclinical models increases intratumoural infiltration of pro-inflammatory immune cells and enhances responses to immunotherapy, leading to decreased tumour progression. Collectively, our findings reveal a therapeutically actionable role of METTL1-directed m7G tRNA methylation in cancer cell translational control and tumour biology.

2023-08-08 | GSE230694 | GEO

Effect of silencing of METTL1 on m7G modification within mRNA of castration-resistant prostate cancer cells LNCaP-AI via m7G AlkAniline-Seq analysis. [m7G]

Project description:Effect of silencing of METTL1 on m7G modification within mRNA of castration-resistant prostate cancer cells LNCaP-AI via m7G AlkAniline-Seq analysis. [m7G]

| PRJNA1000934 | ENA

Effect of silencing of METTL1 oncastration-resistant prostate cancer cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-08-22 | GSE239769 | GEO

Guanosine-7 tRNA methylation steers tRNA-derived fragment biogenesis and translational control in prostate cancer

Project description:Transfer RNAs (tRNAs) are exceptionally subject to modifications, including methylation. While mRNA methylation is emerging as an important regulator of biological and pathological processes in cancer, how post-transcriptional methylation of tRNAs contributes to cancer is largely unknown. Here we show that the RNA N7-methylguanosine (m7G) methyltransferase METTL1 is highly differentially expressed in prostate cancer compared to non-tumour prostate tissues. METTL1 expression regulation is mediated under the oncogenic PI3K-PTEN pathway. Knockdown of METTL1 dramatically inhibits prostate cancer cell growth and tumour progression in vivo. In contrast, overexpression of the wild type but not the catalytically inactive METTL1 potentiates cell growth. Thus, METTL1-mediated methylation is important for prostate tumorigenesis. Mechanistically we find that METTL1 depletion causes loss of m7G tRNA methylation and increases endonucleolytic cleavage of tRNA leading to an accumulation of 5′ tRNA-derived small RNA fragments. 5′ tRNA-derived fragments steer translation control to favour synthesis of key regulators of tumour growth suppression and immune rejection. In summary, our findings uncover a critical function of m7G tRNA methylation in directing translation control in cancer cells with important implications for tumour growth and unveil METTL1 inhibition as a promising anti-cancer therapeutic strategy.

2023-10-24 | PXD030141 | Pride

METTL1 promotes hepatocarcinogenesis via m7G tRNA modification dependent translation control

Project description:N7-methylguanosine (m7G) modification is one of the most prevalent tRNA modifications in human. The precise function and molecular mechanism of m7G tRNA modification in regulation of cancer remain poorly understood. Here we showed that m7G tRNA modification, METTL1 and WDR4 are elevated in hepatocellular carcinoma (HCC) tissues and associated with HCC patient prognosis. Functionally, silencing METTL1 or WDR4 inhibits HCC cell proliferation, migration and invasion, while forced expression of wild type METTL1 but not its catalytic dead mutant promotes HCC progression. Knockdown of METTL1 reduces m7G tRNA modification and decreases m7G modified tRNA expression. Mechanistically, METTL1 depletion selectively decreases the mRNA translation of a subset of oncogenic genes, especially cell cycle and EGFR pathway genes, in m7G-related codon dependent manner. Moreover, in vivo studies using Mettl1 knock-in and knockout mice reveal a critical function of Mettl1 mediated m7G tRNA modifications in promoting hepatocarcinogenesis in the hydrodynamics transfection HCC model. Our work uncovers the critical functions of tRNA m7G modification in regulating cancer mRNA translation and promoting hepatocarcinogenesis, thus provides new insights into role of the mis-regulated tRNA modifications in cancers.

2021-06-26 | GSE174492 | GEO

Mettl1-mediated B cell responses

Project description:Germinal center (GC) response requires increased protein synthesis. We identify the methyltransferase METTL1 as a translational checkpoint during GC responses. Therefore, we immunized mettl1-cko mice and control mice with NP-OVA, and sorted spleen B cells on day 14.

2024-11-01 | PXD057426 | Pride

siRNA-mediated E2F1 and E2F2 silencing in growth-stimulated prostate cancer cells

Project description:To study the effect of siRNA-mediated E2F1 and E2F2 silencing in growth-stimulated prostate cancer cells.

2021-10-14 | GSE172094 | GEO