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Loss of YTHDC1 m6A reading function promotes invasiveness in urothelial carcinoma of the bladder [RIP-seq]

ABSTRACT: Loss of YTHDC1 m6A reading function promotes invasiveness in urothelial carcinoma of the bladder [RIP-seq]

PROVIDER: PRJNA1106402 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28856735_1.fastq.gz	Fastqsanger.gz
	SRR28856735_2.fastq.gz	Fastqsanger.gz
	SRR28856736_1.fastq.gz	Fastqsanger.gz
	SRR28856736_2.fastq.gz	Fastqsanger.gz
	SRR28856737_1.fastq.gz	Fastqsanger.gz

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Loss of YTHDC1 m6A reading function promotes invasiveness in urothelial carcinoma of the bladder [RIP-seq]

Project description:Bladder cancer poses significant clinical challenges due to its high metastatic potential and poor prognosis, especially when it progresses to muscle-invasive stages. Here, we show that the m6A reader YTHDC1 is downregulated in muscle-invasive bladder cancer and is negatively correlated with the expression of epithelial‒mesenchymal transition genes. The functional inhibition or depletion of YTHDC1 increased the migration and invasion of urothelial cells. Integrative analysis of multimodal sequencing datasets provided detailed insights into the molecular mechanisms mediating YTHDC1-dependent phenotypes and identified SMAD6 as a key transcript involved in the invasiveness of urothelial carcinoma of the bladder. Notably, SMAD6 mRNA colocalized less with YTHDC1 in tumoral tissues than in paratumoral tissues, indicating disrupted binding during cancer progression. Our findings establish YTHDC1-dependent m6A reading as a critical epitranscriptomic mechanism regulating bladder cancer invasiveness and provide a paradigm for the epitranscriptomic deregulation of cancer-associated networks.

2024-12-16 | GSE266224 | GEO

Loss of YTHDC1 m6A reading function promotes invasiveness in urothelial carcinoma of the bladder [RNA-seq]

2024-12-16 | GSE266223 | GEO

Loss of YTHDC1 m6A reading function promotes invasiveness in urothelial carcinoma of the bladder [RNA-seq]

Project description:Loss of YTHDC1 m6A reading function promotes invasiveness in urothelial carcinoma of the bladder [RNA-seq]

| PRJNA1106403 | ENA

High throughput sequencing for YTHDC1 binding RNAs [RIP-seq]

Project description:High throughput sequencing for YTHDC1 binding RNAs [RIP-seq]

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Low expression of m6A reader YTHDC1 promotes progression of ovarian cancer via PIK3R1/STAT3/GANAB axis

Project description:We applied YTHDC1-RIP-seq in SKOV3 cells to identify RNAs directly bound to YTHDC1. A total of 9522 potential candidate targets of YTHDC1 were revealed, and 86.39% of them were mRNA

2024-01-01 | GSE238066 | GEO

YTHDC1 m6A-dependent and m6A-independent functions converge to preserve DNA damage response (RIP-seq)

Project description:Cells have evolved a robust and highly regulated DNA damage response to preserve their genomic integrity. Although increasing evidence highlights the relevance of RNA regulation, our understanding of its impact on a fully efficient DNA damage response remains limited. Here, through a targeted CRISPR-knockout screen, we identified RNA binding proteins and modifiers that participate in mediating the p53 response. Among the top hits, m6A reader YTHDC1 was identified as a master regulator of p53 expression. YTHDC1 binds to the transcription start sites ofTP53and other genes involved in DNA damage response, promoting their transcriptional elongation. YTHDC1 deficiency leads to reducedTP53expression, and also retention of introns leading to aberrant protein production of key DNA damage factors. While intron retention is dependent on m6A, YTHDC1 favoursTP53transcriptionalpause-release independently of m6A. Depletion of YTHDC1 causes genomic instability and aberrant cancer cell proliferation mediated by genes regulated by YTHDC1. Our results uncover YTHDC1 as an orchestrator of the DNA damage response through distinct mechanisms of co-transcriptional mRNA regulation.

2024-05-07 | GSE262504 | GEO

High throughput sequencing for YTHDC1 binding RNAs [RIP-seq]

Project description:N6-methyladenoisne (m6A) plays critical roles in many biological processes. However, the function of m6A at the early phase of mammalian development remains poorly understood. Here we show that m6A reader Ythdc1 is required for the proliferation of mouse embryonic stem cells (mESCs) in an m6A-dependent manner and its deletion resets mESCs back to a 2C-like state.

2021-01-24 | GSE146465 | GEO

RNA N6-methyladenosine reader YTHDC1 is essential for TGF-beta-mediated metastasis of triple negative breast cancer [RIP-Seq]

Project description:RNA N6-methyladenosine (m6A) modification and its regulators fine tune gene expression and contribute to tumorigenesis. Here, we uncover the oncogenic role and mechanism of YTHDC1, an m6A reader positively correlated to poor prognosis in breast cancer patients. In a mammary fat pad mouse model, YTHDC1 significantly promoted lung metastasis of triple negative breast cancer (TNBC) cells. Using transcriptome-wide sequencing techniques, we found dysregulation of metastasis-related pathways following YTHDC1 depletion and demonstrated that YTHDC1 is critical for nuclear export of SMAD3 mRNA. YTHDC1 depletion desensitizes TNBC cells to TGF-β, resulting in impaired TGF-β-induced gene signature and inhibition on epithelial-mesenchymal transition (EMT) and cell migration/invasion, which could be at least partially restored by SMAD3 overexpression. Furthermore, we show that the ability of YTHDC1 to recognize m6A on SMAD3 RNA is important for its oncogenic role. Collectively, our study unravels YTHDC1 as vital for distant TNBC metastasis by promoting TGF-β-mediated EMT via SMAD3.

2023-03-25 | GSE193154 | GEO

PAR-CLIP analysis of YTHDC1, SRSF1, SRSF3, SRSF7, SRSF9 and SRSF10 in human HeLa cells

Project description:Label the cells overexpressed Flag tagged YTHDC1, SRSF1, SRSF3, SRSF7, SRSF9 and SRSF10 with 4-SU, the RNA bound by YTHDC1 and SRSF proteins can be got by Flag IP followed by RNA isolation by using the TRIzol (Invitrogen) reagent by following the company manual.the RNA was then used for library preparation using a TruSeqâ¢ RNA Sample Prep Kit v2 (Illumina, San Diego, CA, USA) according to the manufacturerâs protocol.The libraries were sequenced using HiSeq2000 (Illumina) in single-read mode, creating reads with a length of 101 bp. Sequencing chemistry v2 (Illumina) was used and samples were multiplexed in two samples per lane. Discovery of the binding motif of YTHDC1, SRSF1, SRSF3, SRSF7, SRSF9 or SRSF10 in overexpressed Human HeLa cells

2016-02-17 | E-GEOD-71096 | biostudies-arrayexpress

YTHDC1 m6A-dependent and m6A-independent functions converge to preserve DNA damage response (Ythdc1 ChIP-Seq)

2024-05-07 | GSE239331 | GEO