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Knockdown of IGFBP7 decreases FGF2 expression in GC.

ABSTRACT: Knockdown of IGFBP7 decreases FGF2 expression in GC.

PROVIDER: PRJNA854942 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19926134_1.fastq.gz	Fastqsanger.gz
	SRR19926134_2.fastq.gz	Fastqsanger.gz
	SRR19926135_1.fastq.gz	Fastqsanger.gz
	SRR19926135_2.fastq.gz	Fastqsanger.gz

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Knockdown of IGFBP7 decreases FGF2 expression in GC.

Project description:Our previous study reported that IGFBP7 plays a role in maintaining mRNA stability of oncogenic lncRNA UBE2CP3 by RNA-RNA interaction. Clinical cohort studies had implied an oncogenic role of IGFBP7 in GC. However, the molecular mechanism of IGFBP7 in driving gastric cancer (GC) progression remains unknown. In this study, clinical analysis based on two independent cohort showed that IGFBP7 was positively associated with poor prognosis and macrophage infiltration in GC. Loss-of-function studies confirmed the oncogenic properties of IGFBP7 in regulating GC cell proliferation and invasion. Mechanismly, IGFBP7 was induced by epithelial-to-mesenchymal transition (EMT) signaling, since its expression was increased by TGF-beta treatment and reduced by overexpression of OVOL2 in GC. RNA sequencing, qRT-PCR, ELISA assay showed that IGFBP7 positively regulating FGF2 expression and secretion. Transcriptome analysis revealed that FGFR1 was downregulated in M1 macrophages but upregulated in M2 macrophages. Exogenous recombinant IGFBP7 protein in macrophages and GC cells further identified that IGFBP7 promotes macrophage polarization towards to a M2/TAM phenotype via FGF2/FGFR1/PI3K/AKT axis. Our finding highlights that IGFBP7 promotes GC by enhancing TAM infiltration through FGF2/FGFR1/PI3K/AKT axis.

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