OPN Promotes Cell Proliferation and Invasion through NF-κB in Human Esophageal Squamous Cell Carcinoma

Abstract

Background. Osteopontin (OPN) is a phosphorylated glycoprotein. There is increasing evidence that the OPN gene played a major role in the progression of solid organ tumors. However, few studies have clarified how OPN regulated the functional role of human esophageal squamous cell carcinoma (ESCC). This study was designed to investigate the effect of OPN in esophageal squamous cell carcinoma. Methods. First, we screened Eca-109 and KYSE-510 cells to construct OPN silencing and overexpression models. Endogenous OPN of Eca-109 and KYSE-510 were knocked down or overexpressed using small interfering RNAs. QRT-PCR, Western blot, flow cytometry, and CCK-8 were used to detect the function of Eca-109 and KYSE-510 cells. Tumor formation in nude mice was used to measure tumor growth after OPN inhibition. Results. Eca-109 and KYSE-510 cells contain the si-OPN arrest cell cycle in the S-phase and increase apoptosis. These changes were OPN downregulation of the NF-κB pathway that significantly reduced the protein levels of TNF-α, IL-1β, and p-p65. However, the activity of Eca-109 and KYSE-510 cells was enhanced in OPN overexpressing cells. Then, the in vivo tumor formation experiment in nude mice showed that the tumor volume and weight of nude mice after silencing OPN were significantly reduced. Conclusion. This study contributed to understanding the vital role of OPN in ESCC development and progression. This could be a promising molecular target for developing new ESCC diagnostic and therapeutic strategies.