Dendritic cell-specific intercellular adhesion molecule-grabbing nonintegrin-related protein (DC-SIGNR), a type II integral membrane protein and a member of the C-type lectins, has been reported to bind various strains of HIV-1, HIV-2, and simian immunodeficiency virus. Serum DC-SIGNR is not currently available for the detection of non-Hodgkin lymphoma (NHL). Using an enzyme-linked immunosorbent assay (ELISA), we assessed the serum levels of DC-SIGNR in 70 cancer patients and 100 healthy controls. Additionally, using immunohistochemistry, we determined the expression of DC-SIGNR in the lymph nodes. Using the ELISA, low serum levels of DC-SIGNR were detected in the patients (median, 4.513 ng·L(-1); range, 1.066-9.232 ng·L(-1); p = 0.0003). Serum concentrations of DC-SIGNR correlated significantly with age (p = 0.0077) and lactic acid dehydrogenase (p = 0.0046) and β2-microglobulin (p = 0.0491) levels. However, we found no statistically significant correlation between serum DC-SIGNR levels and clinical data such as sex, Ann Arbor stage, B symptoms, and histologic subtypes. Moreover, NHL patients with a lower level of serum DC-SIGNR expression in lymphatic endothelial cells also showed negative immunostaining levels. These results suggest that DC-SIGNR is a biological molecule that may be potentially useful in NHL clinical settings.

Abstract. The aim of this study was to investigate tumor biomarker carbohydrate antigen 724 (CA724) in the serum of patients with carcinomas of the colon and rectum at various clinical stages. Serum was collected from 51 patients with colon carcinoma (CC) and 49 patients with rectal carcinoma (RC). CA724 levels were then measured in the different groups according to site, TNM classification, gender, age and metastastic status of the patients. The statistical significance of the differences between the groups was calculated by non-parametric statistics (Mann-Whitney and Kruskall-Wallis tests). We observed a close association between the serum CA724 levels and tumor migration in colorectal carcinoma (CRC) and opposite variation tendencies of CA724 in the evolution of CC and RC. In conclusion, we identified a close association between the serum levels of CA724 and tumor migration in CRC. The opposite variation tendencies of CA724 in the different evolution groups of CC and RC may reflect the differences between these two types of cancer. The evaluation of serum CA724 may be of monitoring and and predictive value and may also assist in the development of treatment strategies for CRC patients.

Abstract. Colorectal cancer is one of the leading causes of cancer-related mortality, being the third most commonly diagnosed cancer among men and the second among women. Accumulating evidence regarding carbohydrate antigen (CA) demonstrated that tumor-associated antigens are clinically useful for the diagnosis, staging and monitoring of human gastrointestinal cancers, particularly colorectal cancer. There has been an extensive investigation for sensitive and specific markers of this disease. Currently, the gastrointestinal cancer-associated carbohydrate antigen 19-9 (CA19-9) is the most widely applied tumor marker in cancer diagnosis. Despite a similar etiology and cancer incidence rates, there are anatomical and clinical differences between colon and rectal cancer, as well as differences regarding tumor progression and adjuvant treatments. To investigate whether CA19-9 is differentially expressed between colon and rectal cancer, we conducted a differential analysis of serum CA19-9 levels among 227 cases of colorectal cancer, analyzing gender, age, Dukes' stage and distant metastasis for human colon and rectal cancer as a single entity, separately and as matched pairs. We demonstrated that the serum CA19-9 levels in colorectal cancer were upregulated in advanced stages with distant metastasis. By contrast, the serum CA19-9 levels in colon cancer displayed a differential and upregulated behavior in advanced stages with distant metastasis. By analyzing as matched pairs, the upregulated serum CA19-9 levels in rectal cancer during the early stages without distant metastasis further supported our hypothesis that the expression of CA19-9 displays a site-specific differential behavior. The integrative analysis suggested a significant difference between human colon and rectal cancer, justifying individualized therapy for these two types of cancer.

Purpose Our purpose was to verify the effects of atorvastatin (ATO) on prostate cancer (PCa) proliferation, apoptosis, invasion, and metastasis and to further explore the drug’s mechanism of action. Materials and Methods We used cell counting kit-8 (CCK8) and clone formation experiments to study the effect of ATO on the proliferation of PC3 cells. Flow cytometry and Hoechst 33342 staining were used to detect cell apoptosis. Cell migration and invasion were detected through wound healing experiments and transwell experiments. Western blotting was applied to detect apoptosis-related proteins (BAX, Bcl-2, PARP, and Caspase-3), epithelial-mesenchymal transformation (EMT) proteins, and matrix metalloproteinase (MMP) expression. A mouse xenograft tumor model was established, and tumor volume and weight were determined. The expression levels of the above-mentioned proteins were determined through western blot. Results ATO inhibited PC-3 cell proliferation and promoted cell apoptosis in a dose-dependent manner. ATO significantly up-regulated the expression of BAX, PARP, and Caspase-3 and inhibited the expression of Bcl-2. Wound healing and transwell experiments showed that ATO inhibited invasion and metastasis in PC-3 cells, possibly because ATO could inhibit the EMT and the expression of MMPs in PC-3 cells. Studies in nude mice showed that ATO significantly reduced tumor volume and weight; the expression levels of related proteins were consistent with the in vitro results. Conclusions ATO inhibits the occurrence and development of PCa and regulates the migration and invasion of PCa cells by inhibiting the EMT and MMPs.

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