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Background: The relationship of inflammation and tumor is becoming more and more important in the study on the pathogenesis of colorectal cancer. The role of TLR9-mediated immune inflammation reaction in the process is not currently clear. The purpose of the study was to discuss the correlation of TLR9 signal activation with tumor progression by detecting the expression of TLR9 and its downstream molecule NF-kappaB in colorectal cancer tissues at different stages. Methods: TLR9 expression in colorectal cancer tissues was detected by immunohistochemical streptavidin-perosidase method and Western blot. Results: The result showed that the high expression of TLR9 was correlated with tumor poorly differentiation, invasion and liver metastasis, the abnomal increasing levels of CEA in blood. With the signal activation, the levels of TLR9 protein raised more in advanced colorectal cancer than in early colorectal cancer. Afterward, we found that the activation of specific expression of TLR9 signal was related to histologic origin. TLR9-C expression displayed in both advanced cancer and para-carcinoma tissues, and TLR9-R protein was predominat in partial sigmoid and rectal cancer tissues. With the differential expression of TLR9, the levels of its downstream molecule NF-kappaB protein increased in colon cancer tissues and decreased in rectal cancer tissues. Conclusion: The results confirmed that TLR9 signaling activation participated in the clinical process of colorectal cancer and influenced NF-kappaB expression. [ABSTRACT FROM AUTHOR]

Background: The beneficial antitumor effects of low-molecular-weight heparins (LMWHs) have previously been investigated in basic and clinical studies. In this study, the antitumor efficacy of nadroparin combined with radiotherapy was investigated in vivo. Methods: A total of 48 tumor-bearing mice were randomly divided into six groups (n=8 per group): control group, irradiation group (X), LMWH1,000 group, LMWH2,000 group, LMWH1,000+ X group and LMWH2,000+X group. Following this, tumor growth, weight and inhibitory rate, as well as the survival of mice in each group, were determined. Levels of serum interleukin (IL)-6 and transforming growth factor (TGF)-β1 were determined via enzyme-linked immunosorbent assay (ELISA) analyses. The expression levels of CD34 were investigated using immunohistochemistry analyses to represent the microvascular density (MVD) values of tumor tissues. In addition, tumor cell apoptosis was investigated using TdT-mediated dUTP nick end labeling (TUNEL) analysis post treatment. The expression levels of survivin were analyzed by Western blotting. Results: The volumes and weights of tumors in the treatment groups were demonstrated to be significantly decreased, which was most obvious in the LMWH2,000+X group. The tumor inhibitory rate was significantly increased in the treated mice. ELISA assays demonstrated that the concentrations of serum IL-6 and TGF-β1 were significantly decreased in the LMWH2,000+ X group. In addition, the decreased CD34 expression was found in the combined treatment groups. TUNEL assays demonstrated that the apoptosis rate was increased in treated mice, and the highest apoptosis rate was exhibited by the LMWH2,000+X group. Results of Western blotting demonstrated that combinatory treatment with both nadroparin and X-ray irradiation significantly inhibited the expression of survivin. Conclusion: These results demonstrated that a combinatory treatment strategy of nadroparin with fractionated irradiation had a strong synergistic antitumor effect in vivo, which may be associated with the promotion of apoptosis, inhibited secretion of TGF-β1 and IL-6 and downregulation of CD34 and survivin expression. [ABSTRACT FROM AUTHOR]