Yu-Xiu Yang

Epithelial-mesenchymal transition during oncogenic transformation induced by hexavalent chromium involves reactive oxygen species-dependent mechanism in lung epithelial cells.

Hexavalent chromium [Cr(VI)] is an important human carcinogen associated with pulmonary diseases and lung cancer. Exposure to Cr(VI) induces DNA damage, cell morphological change and malignant transformation in human lung epithelial cells. Despite extensive studies, the molecular mechanisms remain elusive, it is also not known if Cr(VI)-induced transformation might accompany with invasive properties to facilitate metastasis. We aimed to study Cr(VI)-induced epithelial-mesenchymal transition (EMT) and invasion during oncogenic transformation in lung epithelial cells. The results showed that Cr(VI) at low doses represses E-cadherin mRNA and protein expression, enhances mesenchymal marker vimentin expression and transforms the epithelial cell into fibroblastoid morphology. Cr(VI) also increases cell invasion and promotes colony formation. Further studies indicated that Cr(VI) uses multiple mechanisms to repress E-cadherin expression, including activation of E-cadherin repressors such as Slug, ZEB1, KLF8 and enhancement the binding of HDAC1 in E-cadherin gene promoter, but DNA methylation is not responsible for the loss of E-cadherin. Catalase reduces Cr(VI)-induced E-cadherin and vimentin protein expression, attenuates cell invasion in matrigel and colony formation on soft agar. These results demonstrate that exposure to a common human carcinogen, Cr(VI), induces EMT and invasion during oncogenic transformation in lung epithelial cells and implicate in cancer metastasis and prevention.

Outcomes of autologous bone marrow mononuclear cell transplantation in decompensated liver cirrhosis.

AIM To determine the long-term efficacy of autologous bone marrow mononuclear cells (BM-MNCs) transplantation in terms of improving liver function and reducing complications in patients with decompensated cirrhosis. METHODS A total of 47 inpatients with decompensated liver cirrhosis were enrolled in this trial, including 32 patients undergoing a single BM-MNCs transplantation plus routine medical treatment, and 15 patients receiving medical treatment only as controls. Forty-three of 47 patients were infected with hepatitis B virus. Bone marrow of 80-100 mL was obtained from each patient and the BM-MNCs suspension was transfused into the liver via the hepatic artery. The efficacy of BM-MNCs transplantation was monitored during a 24-mo follow-up period. RESULTS Liver function parameters in the two groups were observed at 1 mo after BM-MNCs transfusion. Prealbumin level was 118.3 ± 25.3 mg/L vs 101.4 ± 28.7 mg/L (P = 0.047); albumin level was 33.5 ± 3.6 g/L vs 30.3 ± 2.2 g/L (P = 0.002); total bilirubin 36.9 ± 9.7 mmol/L vs 45.6 ± 19.9 mmol/L (P = 0.048); prothrombin time 14.4 ± 2.3 s vs 15.9 ± 2.8 s (P = 0.046); prothrombin activity 84.3% ± 14.3% vs 74.4% ± 17.8% (P = 0.046); fibrinogen 2.28 ± 0.53 g/L vs 1.89 ± 0.44 g/L (P = 0.017); and platelet count 74.5 ± 15.7 × 10(9)/L vs 63.3 ± 15.7 × 10(9)/L (P = 0.027) in the treatment group and control group, respectively. Differences were statistically significant. The efficacy of BM-MNCs transplantation lasted 3-12 mo as compared with the control group. Serious complications such as hepatic encephalopathy and spontaneous bacterial peritonitis were also significantly reduced in BM-MNCs transfused patients compared with the controls. However, these improvements disappeared 24 mo after transplantation. CONCLUSION BM-MNCs transplantation is safe and effective in patients with decompensated cirrhosis. It also decreases the incidence of serious complications.

Plasma minichromosome maintenance complex component 6 is a novel biomarker for hepatocellular carcinoma patients

This study aimed to investigate the presence of plasma minichromosome maintenance complex component 6 (MCM6) mRNA and protein levels in hepatocellular carcinoma (HCC) patients and evaluate their diagnostic value for HCC.

A preliminary study of plasma cyclase-associated protein 2 as a novel biomarker for early stage and alpha-fetoprotein negative hepatocellular carcinoma patients.

BACKGROUND AND OBJECTIVE Cyclase-associated protein 2 (CAP2) has recently been suggested to be a candidate biomarker for hepatocellular carcinoma (HCC). We aim to investigate the application of CAP2 as a novel biomarker for HCC patients especially for those at early stage and are AFP-negative. METHODS The CAP2 and AFP plasma levels were analyzed by enzyme-linked-immunosorbent assay in 86 HCC, 59 cirrhotic patients, and 30 normal individuals. Their correlation with HCC tumor behavior, disease stages, diagnostic sensitivity, specificity and accuracy were analyzed. RESULTS The results showed that both CAP2 and AFP plasma levels in HCC patients were significantly elevated when compared to cirrhosis and controls. CAP2 levels correlate well with HCC patients histological grade, clinical stage and tumor size, but not with patients age, gender, hepatitis B virus infection status and plasma AFP level. CAP2 had better sensitivity as compared to AFP (82.6% vs 59.3%) for general HCC, and early stage of HCC patients (78.6% vs 40.4%). In addition, CAP2 is able to complement AFP to predict 82.9% of HCC in AFP-negative patients. CONCLUSION We suggest that CAP2 is a novel biomarker for HCC patient, this may be especially useful for detection of early stage HCC and when plasma AFP level is negative.

Helicobacter pylori infection-induced H3Ser10 phosphorylation in stepwise gastric carcinogenesis and its clinical implications.

Our previous works have demonstrated that Helicobacter pylori (Hp) infection can alter histone H3 serine 10 phosphorylation status in gastric epithelial cells. However, whether Helicobacter pylori‐induced histone H3 serine 10 phosphorylation participates in gastric carcinogenesis is unknown. We investigate the expression of histone H3 serine 10 phosphorylation in various stages of gastric disease and explore its clinical implication.