The effects of NF-κB signal pathway on the process of anastomotic stricture after the radical resection of esophageal carcinoma

Abstract

The aim of this article is to identify the relationship between the nuclear factor κB (NF-κB) signal pathway expression and the anastomotic stricture. It particularly focuses on the expression of p65, bcl-2, and cIAP-1 in the anastomotic stricture formation after radical resection of esophageal cancer. A total of 82 esophageal squamous carcinoma patients who had undergone esophagectomy by Ivor Lewis procedure were enrolled in the study. Tissues were collected from the patients who developed the anastomotic stricture after the operation, while para anastomotic tissues served as the control. The protein expression of p65, bcl-2, and cIAP-1 was analyzed by immunohistochemistry and western blot analyses, while the messenger RNA (mRNA) levels of p65, bcl-2, and cIAP-1 were evaluated by reverse transcription polymerase chain reaction (RT-PCR). The results showed that lower expression of p65, bcl-2, and cIAP-1 proteins was observed in the para anastomotic tissue; in the esophageal stricture’s tissue, the expression of these proteins was significantly higher ( P < 0.05). The mRNA levels of P56, bcl-2, and cIAP-1 in the stricture tissue were remarkably increased ( P < 0.05) compared with the para anastomotic tissues, and the mRNA levels in the sample of grade 3 dysphagia were higher ( P < 0.05) than the levels of grade 1 and 2. In the normal esophageal epithelial cell of stricture patients was upregulated compared with that of no stricture patients. We can confirm that the anastomotic stricture has the relationship with the NF-κB signal pathway. The bcl-2 and cIAP-1, located downstream of NF-κB signal pathway, could be a new preventive and therapeutic target for the anastomotic stricture.