ABSTRACT: The aim of this study was to investigate the association of survivin expression with metastasis of colorectal cancer (CRC).
RT-PCR and Western blot assays were performed to detect survivin expression in CRC cells and normal intestinal epithelial cell. The expression of survivin gene was also detected in 15 CRC tissues, surrounding and adjacent colon tissues. Moreover, survivin expression in 48 CRC tissues with or without lymph node metastasis was analyzed. Multivariate analysis for lymph node metastasis was performed using logistic regression model. RNA interference was used to inhibit survivin expression in CRC cells and analyze its effect on invasion and metastasis of CRC cells.
The expression levels of survivin mRNA and protein were higher in CRC cells than in normal intestinal epithelial cell line. The average levels of survivin mRNA and protein were higher in CRC tissues than surrounding or adjacent colon tissues (P < 0.05). High survivin expression was an independent factor for predicting lymph node metastasis of CRC (P = 0.043). RNAi-mediated survivin knockdown could significantly inhibit in vitro invasion and in vivo metastasis of CRC cells, which might be inactivation of matrix metalloproteinases.
Targeting survivin will be a potential strategy to suppress metastasis of CRC.
Journal of Surgical Oncology 11/2011; 105(6):520-8. · 2.10 Impact Factor
06/2011; , ISBN: 978-953-307-412-2
ABSTRACT: Gastric carcinoma (GC) remains one of most serious malignant tumors worldwide, with Helicobacter pylori being the definite carcinogen. The H. pylori components, cytotoxin-associated gene A (CagA), vacuolating toxin A (VacA) and blood-group antigen-binding adhesin gene (BabA), can mimic and bind to specific receptors or surface molecules both on gastric epithelial cells and platelets, in which CagA and VacA may also be directly involved in loosening of tight junctions in monolayers of polarized gastric epithelial cells. It has been shown that a history of H. pylori infection is found in the majority of patients with GC, and that anti-CagA, anti-VacA and anti-BabA antibodies targeting both H. pylori components and host mimic molecules can be detected in them with increased levels. Patients with GC who are positive for H. pylori prospectively have a better outlook than those negative. The stimulation of mentioned autoantibodies in antigen processing and presentation and subsequent T-cell activation and proliferation improves host immune status. On the other hand, in an autoimmune response, autoantibodies can induce the cross-reaction against those localized or circulating GC cells, which are characterized by mimic or absorbed H. pylori antigens, and lead to the killing and even suppressing of metastasis of cancer cells. Therefore, we here hypothesize that autoimmune responses induced by H. pylori components may play a key role in improving the prognosis of patients with gastric carcinoma.
Medical Hypotheses 02/2008; 70(2):273-6. · 1.39 Impact Factor