A Disintegrin and metalloproteinase 17 (ADAM17) was proposed to cooperate with NF-κB p65, promoting tumorigenesis and progression of several human cancers. However, the role of ADAM17 remains unknown in human esophageal squamous cell carcinoma (ESCC). In this study, gene expression analyses and cell viability assays suggested that knockdown of ADAM17 suppressed ESCC cell viability. Gene expression analyses and ChIP-qPCR revealed that NF-κB p65 positively regulated ADAM17 expression by binding to the ADAM17 promoter. Rescue experiments showed that overexpression of ADAM17 in NF-κB p65-depleted ESCC cells restored cell viability. In addition, western blot analyses and ChIP-qPCR indicated that ADAM17 was responsible for the persistent activation of NF-κB p65 and contributed to ADAM17 expression in ESCC cells. In conclusion, we propose that ADAM17-activated NF-κB p65 signaling positively regulates ADAM17 expression, and facilitates ESCC cell viability.
Keywords: ADAM17; ESCC; NF-κB p65; cell viability.
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