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

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

PROVIDER: PRJNA834060 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19033245_1.fastq.gz	Fastqsanger.gz
	SRR19033245_2.fastq.gz	Fastqsanger.gz
	SRR19033246_1.fastq.gz	Fastqsanger.gz
	SRR19033246_2.fastq.gz	Fastqsanger.gz
	SRR19033247_1.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:RNA m6A reader IGF2BP3 promotes metastasis of triple-negative breast cancer via SLIT2 repression (MeRIP-Seq)

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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

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Effect of depletion of IGF2BP3 on gene expression in LUAD

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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IGF2BP3 Promotes Stemness and Leukemogenesis in Acute Myeloid Leukemia

Project description:N6-methyladenosine (m6A) is the most abundant internal modification in mRNA, and its modulators have been implicated in various biological processes. Here, we demonstrate that the mRNA m6A reader IGF2BP3 is highly expressed in human acute myeloid leukemia (AML), particularly in AML leukemia stem/initiating cells (LSCs/LICs). IGF2BP3 is required for the development and maintenance of AML and the self-renewal of LSCs/LICs but dispensable for normal hematopoiesis. IGF2BP3 exhibits promising anti-AML efficacy both in vitro and in vivo, providing new therapeutic strategies for targeting AML.

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IGF2BP3 controls cancer cell invasiveness by modulation RISC function

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