当前位置： SCI文献检索 > BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS期刊下所有文献 > Radiation-induced IL-1β expression and secretion promote cancer cell migration/invasion via activation of the NF-κB-RIP1 pathway.

Radiation-induced IL-1β expression and secretion promote cancer cell migration/invasion via activation of the NF-κB-RIP1 pathway.

Abstract：

:Here, we demonstrate that interleukin-1β (IL-1β) contributes to the γ-ionizing radiation (IR)-induced increase of migration/invasion in A549 lung cancer cells, and that this occurs via RIP1 upregulation. We initially observed that the protein expression and secreted concentration of IL-1β were increased upon exposure of A549 cells to IR. We then demonstrated that IR-induced IL-1β is located downstream of the NF-κB-RIP1 signaling pathway. Treatments with siRNA and specific pharmaceutical inhibitors of RIP1 and NF-κB suppressed the IR-induced increases in the protein expression and secreted concentration of IL-1β. IL-1Ra, an antagonist of IL-1β, treatment suppressed the IR-induced epithelial-mesenchymal transition (EMT) and IR-induced invasion/migration in vitro. These results suggest that IL-1β could regulate IR-induced EMT. We also found that IR could induce the expression of IL-1β expression in vivo and that of IL-1 receptor (R) I/II in vitro and in vivo. The IR-induced increases in the protein levels of IL-1 RI/II and IL-1β suggest that an autocrine loop between IL-1β and IL-1 RI/II might play important roles in IR-induced EMT and migration/invasion. Based on these collective results, we propose that IR concomitantly activates NF-κB and RIP1 to trigger the NF-κB-RIP1-IL-1β-IL-1RI/II-EMT pathway, ultimately promoting metastasis.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Kang AR,Cho JH,Lee NG,Kwon JH,Song JY,Hwang SG,Jung IS,Kim JS,Um HD,Oh SC,Park JK

doi

10.1016/j.bbrc.2020.10.057

subject

Has Abstract

pub_date

2021-01-01 00:00:00

pages

973-979

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(20)31980-X

journal_volume

534

pub_type

杂志文章

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