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

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

PROVIDER: PRJEB52408 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR9627490_1.fastq.gz	Fastqsanger.gz
	ERR9627490_2.fastq.gz	Fastqsanger.gz
	ERR9627500_1.fastq.gz	Fastqsanger.gz
	ERR9627500_2.fastq.gz	Fastqsanger.gz
	ERR9627491_1.fastq.gz	Fastqsanger.gz

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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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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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METTL3 modulates cell viability and motility in HCC1143 and MDA-MB-231 triple-negative breast cancer cell lines

Project description:The m6A methyltransferase METTL3 functions as a critical oncogenic driver in triple negative breast cancer (TNBC). However, its specific downstream targets and mechanistic functions in less metastatic TNBC subtypes remain poorly characterized. To address this, we evaluated METTL3 expression and the phenotypic effects of its siRNA-mediated knockdown in healthy mammary epithelial (MCF10A), low-metastatic TNBC (HCC1143) and high-metastatic TNBC (MDA-MB-231) cell lines. We assessed global m6A levels, cell proliferation, cell cycle progression and migration. To uncover specific downstream pathways, transcriptomic profiling was performed on HCC1143 cells, followed by RT-qPCR validation and m6A site prediction. METTL3 depletion reduced global m6A levels and cell viability across all cell lines. Notably, in low-metastatic HCC1143 cells, METTL3 knockdown induced a pronounced G2/M cell cycle arrest and dramatically impaired migration capacity. Transcriptomic analysis of HCC1143 revealed altered expression of genes associated with these observed phenotypic changes. Specifically, critical transcripts harboring predicted m6A motifs, including LIMK1, CCNB2 and CDH1, were significantly dysregulated, pointing to potential alterations in pathways governing cytoskeletal remodeling, actin organization, and cell-cell adhesion. Taken together, we propose that METTL3 promotes cellular proliferation and motility in low-metastatic TNBC by regulating key transcripts involved in cell cycle progression and actin dynamics.

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Methyltransferase-like 3 (METTL3) regulates exocytosis

Project description:RNA modification pathways are often mis-regulated in various typers of cancer, with N6-methyladenosine (m6A) playing a pivotal role in cancer progression and metastasis. Methyltransferase-like 3 (METTL3), a core component of the m6A methyltransferase complex, functions not only as an m6A writer but also promotes tumorigenesis through m6A-independent mechanisms. Here, we show that METTL3 is mislocalized to the cytoplasm in breast cancer tumors from patients, contributing to the oncogenic phenotype. Cytoplasmic METTL3 interacts with EXOC7, a key exocytosis regulator. Additionally, METTL3 regulates m6A-dependent alternative splicing (AS) of EXOC7, promoting the expression of a more aggressive isoform. Silencing METTL3 impairs vesicle trafficking and alters the breast cancer secretome. These effects arenot dependent on its enzymatic activity but instead associated with METTL3-mediated stabilization of EXOC7. Furthermore, knockdown of METTL3 , but not inhibition of its catalytic function, impairs invadopodia formation, collagen matrix invasion, and the generation of focal adhesions , all of which are critical for extracellular matrix degradation and cell invasion. Our findings uncover non-catalytic roles of METTL3 in regulating exocytosis and the cancer secretome, with broader implications for other cancer types.

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Breast cancer cell lines

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Transcriptome analysis of gene expression in scramble and METTL3 Knockdown HUVEC cell lines

Project description:We have used RNA-seq to explore gene expression profiles in scramble and METTL3 Knockdown HUVEC cell lines.

2021-12-01 | GSE157544 | GEO

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Project description:This study investigates transcriptomic changes induced by METTL3 knockdown in ovarian cancer cells. RNA-seq was performed on METTL3-kd (SM) and control (NC) samples to profile gene expression alterations.

2026-02-18 | GSE313200 | GEO

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