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Interaction between oncogenic FREM2 with IL-1β signaling contributes to esophageal squamous cell carcinoma progression

ABSTRACT: Inflammatory signals can promote tumorigenesis. The pro-inflammatory cytokine interleukin (IL)-1β is overexpressed in many types of tumor; however, it is unclear whether it directly interacted with oncogenes in esophageal squamous cell carcinoma. In this study, we performed RNA sequencing to identify tumorgenesis and recurrence-related factors in ESCC and identified FRAS1-related extracellular matrix protein (FREM)2 as a candidate oncogene. IL-1β and IL-1R1 were upregulated in ESCC tissue, which was accompanied by elevated Frem2 expression. FREM2 formed complex with IL-1R1 at the cell surface and promoted ESCC cell proliferation and migration via activation of nuclear factor-κB–p65/mitogen-activated protein kinase–c-Jun N-terminal kinase signaling. IL-1β stimulation resulted in the upregulation of FREM2 in ESCC cells through inhibition of Forkhead box P1. Increased FREM2 and IL-1R1 levels were correlated with shorter survival time in ESCC patients.

ORGANISM(S): Homo sapiens

PROVIDER: GSE119436 | GEO | 2019/09/03

REPOSITORIES: GEO

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Gene regulation by IL-1β in IL-1R1-deficient mixed glia

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2006-03-25 | GSE4507 | GEO

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2012-06-22 | GSE33755 | GEO

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Mus musculus

Project description:Gene regulation by IL-1β in IL-1R1-deficient mixed glia

| PRJNA94503 | ENA