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RNA m6A reader IGF2BP3 promotes metastasis of triple-negative breast cancer via SLIT2 repression (MeRIP-Seq)

ABSTRACT: RNA m6A reader IGF2BP3 promotes metastasis of triple-negative breast cancer via SLIT2 repression (MeRIP-Seq)

PROVIDER: PRJNA835101 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19086277.fastq.gz	Fastqsanger.gz
	SRR19086278.fastq.gz	Fastqsanger.gz
	SRR19086279.fastq.gz	Fastqsanger.gz
	SRR19086280.fastq.gz	Fastqsanger.gz

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RNA m6A reader IGF2BP3 promotes metastasis of triple-negative breast cancer via SLIT2 repression (MeRIP-Seq)

Project description:Triple-negative breast cancer (TNBC) is a group of fatal malignancies characterized by high metastatic capacity, the underlying mechanisms of which remain largely elusive. We found here that insulin-like growth factor 2 mRNA binding protein 3 (IGF2BP3), but not other members of the IGF2BP family, is highly expressed in breast cancer and correlated clinically with TNBC metastasis and patient prognosis. IGF2BP3 promotes the migration and invasion capabilities of TNBC cells dependent upon cellular RNA N6-methyladenosine (m6A) modification. Mechanistically, IGF2BP3 binds to and unstabilizes m6A-methylated mRNA of the extracellular matrix glycoprotein, SLIT2, impairs its downstream signaling via the cognate receptor ROBO1, and consequently derepresses the canonical oncogenic PI3K/AKT and MEK/ERK pathways. These findings shed light into the regulatory network of distal metastasis and provide rationale for targeting the m6A machinery in the treatment of TNBC

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RNA m6A reader IGF2BP3 promotes metastasis of triple-negative breast cancer via SLIT2 repression

Project description:RNA m6A reader IGF2BP3 promotes metastasis of triple-negative breast cancer via SLIT2 repression

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Project description:YTHDC1 is one of m6A reader proteins exerting multifaceted effects on determining the fate of m6A RNA within the nucleus and highly expressed in liver cancer cells.To understand how YTHDC1 contributes to liver cancer progression, we conducted MeRIP-seq assay in HepG2 cells and aimed to identified YTHDC1 target transcripts.

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Project description:IGF2BP3, an oncofetal protein and an m6A reader, is a member of the IGF2BPs family playing an important role in cell migration in early embryogenesis, oncogenesis, metabolism and metastasis. To clarify the effect of depletion of IGF2BP3 on gene expression in LUAD, we conducted IGF2BP3 knocked out experiments in the NCI-H1299 LUAD cell lines. The knockout efficiency was validated by western blot analysis, demonstrating successful silencing of IGF2BP3 at the protein levels in NCI-H1299 cells. To explore the underlying mechanisms of IGF2BP3 in LUAD development, we conducted RNA-sequencing analysis using IGF2BP3 knockout and control NCI-H1299 cells, with each group consisting of three biological replicates. The analysis revealed that IGF2BP3 knockout resulted in differential expression of 1700 genes including 621 genes upregulated and 1079 downregulated.

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