Anti-DNM3 (internal region) polyclonal antibody

Background: Primary hepatocellular carcinoma is one of the most common malignant tumors in China and its mortality rate shows no sign at present of ceasing to rise. In our previous study, we found that the mRNA level of Dynamin3 (DNM3), a member of the Dynamin family, is significantly lower in hepatocellular carcinoma tissues than in non-tumor tissues. The aim of this study was to investigate the expression pattern and potential function of DNM3 in hepatocellular carcinoma. Material/Methods: First, we determined the expression of DNM3 in human hepatocellular carcinoma tissues and cell lines. We then studied the biological function of DNM3 on hepatocellular carcinoma cells by proliferation assay and colony formation assay. Flow cytometry was used to study the effect of DNM3 on cell cycle and apoptosis. Results: Expression of DNM3 was significantly downregulated in hepatocellular carcinoma tissues and was associated with vein invasion and tumor metastasis. In addition, upregulation of DNM3 reduced hepatocellular carcinoma cell proliferation and colony formation, induced hepatocellular carcinoma cell G0/G1 phase arrest, and stimulated hepatocellular carcinoma cell apoptosis. We also found that DNM3 may exert its anti-proliferative effect through upregulating p53. Conclusions: Our findings suggest that DNM3 attenuates the proliferation and induces apoptosis of gastric cancer cells. Modulation of DNM3 may prove to be an efficient method of hepatocellular carcinoma treatment.

Differentiation between Sezary syndrome and erythrodermic inflammatory dermatoses can be challenging, and a number of studies have attempted to identify characteristic immunophenotypic changes and molecular biomarkers in Sezary cells that could be useful as additional diagnostic criteria. In this European multicenter study, the sensitivity and specificity of these immunophenotypic and recently proposed but unconfirmed molecular biomarkers in Sezary syndrome were investigated. Peripheral blood CD4(+) T cells from 59 patients with Sezary syndrome and 19 patients with erythrodermic inflammatory dermatoses were analyzed for cell surface proteins by flow cytometry and for copy number alterations and differential gene expression using custom-made quantitative PCR plates. Experiments were performed in duplicate in two independent centers using standard operating procedures with almost identical results. Sezary cells showed MYC gain (40%) and MNT loss (66%); up-regulation of DNM3 (75%), TWIST1 (69%), EPHA4 (66%), and PLS3 (66%); and down-regulation of STAT4 (91%). Loss of CD26 (>= 80% CD4(+) T cells) and/or CD7 (>= 40% CD4(+) T cells) and combination of altered expression of STAT4, TWIST1, and DNM3 or PLS3 could distinguish, respectively, 83% and 98% of patients with Sezary syndrome from patients with erythrodermic inflammatory dermatoses with 100% specificity. These additional diagnostic panels will be useful adjuncts in the differential diagnosis of Sezary syndrome versus erythrodermic inflammatory dermatoses.