DPP3 expression promotes cell proliferation and migration in vitro and tumour growth in vivo, which is associated with poor prognosis of oesophageal carcinoma.

Dipeptidyl peptidase III (DPP3), a zinc­dependent metallopeptidase, is upregulated in a variety of malignancies. However, little is known about its roles in the pathogenesis of these malignancies. The present study was designed to investigate the roles of DPP3 in the pathogenesis and progression of oesophageal cancer (EC). The expression level of DPP3 in EC tissues and adjacent normal tissues was detected in 93 cases of tissue biopsies collected from patients diagnosed with oesophageal carcinoma by immunohistochemistry. The effect of DPP3 expression on cell proliferation, migration or apoptosis was determined in DPP3­depleted EC cells created by infection with lentivirus containing short hairpin RNA specific to the human DPP3 mRNA sequence, followed by detection at the cellular level using a Celigo cell count assay, flow cytometry, wound­healing assay and Transwell assay as well as chip screening with a Human Apoptosis Antibody Array kit, which enables the quantitative detection of 43 apoptosis­related genes. A xenograft model was applied to detect the tumour growth and invasion of DPP3­depleted cancer cells in nude mice. The results revealed that DPP3 expression was elevated in EC tissues compared with adjacent non­tumour tissues, and high DPP3 expression was significantly associated with poor prognosis. DPP3 depletion resulted in reduced cell proliferation and migration and enhanced cell cycle arrest and apoptosis of EC cells and led to the inhibition of tumour growth and invasion in a xenograft model. In addition, DPP3 depletion was associated with the upregulation of the proapoptotic proteins SMAC and p53 and the downregulation of the antiapoptotic proteins clAP­2, IGFBP­2 and TRAILR­4. Finally, DPP3 may promote cell proliferation, migration and survival of EC cells in vitro and tumour growth and invasion of oesophageal carcinoma in vivo, and thus may serve as a molecular target for tumour therapy.

Comparison of the clinical characteristics and survival between Uyghur patients with hepatitis virus-related and non-B, non-C hepatocellular carcinoma in Xinjiang, China.

OBJECTIVE: To compare the clinical characteristics and prognosis between hepatitis virus-related hepatocellular carcinoma (viral HCC) and non-B, non-C HCC (NBC-HCC) among Uyghur patients in Xinjiang province, China. METHODS: Between 01/01/2000 and 31/12/2012, 319 Uyghur HCC patients were treated at the Cancer Centre of The First Affiliated Hospital of Xinjiang Medical University. The data for the patients were obtained from a retrospective review of the patients' medical records. A total of 18 patients were excluded from the study because of incomplete information. The patients were classified into two groups: viral HCC and NBC-HCC. The clinical characteristics and prognostic factors were statistically analysed. RESULTS: For all 301 patients, gender (P=0.000), area of residence (P=0.002), diabetes mellitus (P=0.009), BMI (P=0.000), cirrhosis (P=0.000), tumour stage (P=0.004), Child-Pugh class (P=0.000), the TBIL level (P=0.000), and the alpha-fetoprotein (AFP) level (P=0.000) were significantly different between the NBC-HCC and viral HCC groups. The NBC-HCC patients tended to be diagnosed at advanced stages; however, the NBC-HCC patients exhibited lower Child-Pugh scores than the viral HCC patients. In all patients examined, the 0.5-, 1-, 3- and 5-year overall survival (OS) rates were 35.6%, 20.3%, 12.6% and 4.5%, respectively. No significant difference in OS was observed between the two groups (P=0.124). Cox multivariate analysis revealed that age (RR =1.539, P=0.001), TNM stage (RR =12.708, P=0.000), portal vein tumour thrombus (PVTT) (RR =2.003, P=0.000), Child-Pugh class (RR =1.715, P=0.000), and TACE + radiotherapy/RFA (RR =0.567, P=0.000) were significant independent prognostic factors for HCC patients. CONCLUSIONS: The clinical characteristics differ between Uyghur patients with NBC-HCC and viral HCC. HCC in the Xinjiang region displays specific regional characteristics. Age, TNM stage, PVTT, Child-Pugh class and TACE + radiotherapy/RFA are significant risk factors that influence patient survival.

Clinical significance and diagnostic value of Golgi-protein 73 in patients with early-stage primary hepatocellular carcinoma / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To explore the clinical significance and diagnostic value of GP73 in early-stage primary hepatocelluar carcinoma (PHC).</p><p><b>METHODS</b>GP73 levels in 50 healthy controls, 65 cases of liver cirrhosis and 40 early stage PHC were detected by ELISA. The areas under ROC, sensitivities and specificities were also compared. The relationship between GP73 and liver function parameters was analyzed.</p><p><b>RESULTS</b>The median of serum GP73 in early PHC was 291.3 µg/L, significantly higher than that in the cirrhosis group 211.8 µg/L and in the control group 58.3 µg/L (all P<0.01). The sensitivity of GP73 (72.5%) was significantly higher than that of AFP (50.0%), P<0.05. The specificity of GP73 (70.4%) was lower than that of AFP (95.7%), P<0.05. The sensitivity and specificity in combination for diagnosis were 77.5% and 79.1%, and the area under ROC curve in the combining form was 0.838 (95% CI:0.760-0.917). In the early PHC patients, the median of GP73 in the Child C group was 365.2 µg/L, significantly higher than that in the Child B group 310.6 µg/L and Child A group 266.4 µg/L, P = 0.002. In patients with liver cirrhosis, the median of GP73 in the Child B group was 307.3 µg/L, significantly higher than that in the Child A group 176.6 µg/L, P = 0.031. The level of serum GP73 was positively correlated with ALT, AST, negatively with ABL, A/G, and with no significant correlation with AFP, TBLB, DBLB, IBLB, and GGT.</p><p><b>CONCLUSIONS</b>GP73 has a superior sensitivity in detecting early-stage PHC in liver cirrhosis patients. The sensitivity can be further increased by combining with AFP. The changes of GP73 expression may be related with the decline of liver function.</p>