Maspin expression was involved in colorectal adenoma-adenocarcinoma sequence and liver metastasis of tumors.

Abstract

BACKGROUND: Maspin, a serine protease inhibitor related to the serpin family, can inhibit invasion and metastasis of malignancies. This study aimed to explore the roles of maspin expression in the tumorigenesis and progression of colorectal adenocarcinoma (CRA). MATERIALS AND METHODS: Maspin expression was examined on tissue microarrays containing CRAs (n = 119), adjacent adenoma (n = 22), adjacent non-cancerous mucosa (n = 118) and metastases (n = 67) by immunostaining. Microvessel density (MVD) was determined after labeling with anti-CD34 antibody using immunnostaining. The maspin expression was compared with clinicopathological parameters of the tumors, including expression of p53, Ki-67 and tenascin, MVD, and survival data. RESULTS: Maspin expression showed significant increase from colorectal non-cancerous mucosa to adenocarcinoma through adenoma (p < 0.05). Maspin expression correlated negatively with liver metastasis of CRA (p < 0.05), positively with tenascin expression (p < 0.05), but not with tumor size, depth of invasion, local invasion via vessels, lymph node metastasis, differentiation, expression of Ki-67 and p53 or MVD (p > 0.05). Maspin expression in the metastases of CRA was significantly consistent with their corresponding primary foci (p < 0.05). Kaplan-Meier analysis revealed no significant relationship between maspin expression and survival time of carcinoma patients (p > 0.05). CONCLUSION: Up-regulated maspin expression was involved in colorectal adenoma-adenocarcinoma sequence. Low maspin expression is closely linked to the liver metastasis of CRA possibly through degradation of the extracellular matrix-tenascin to enhance carcinoma cell mobility.