Bin Wang

Background: Past work has established that human glioblastomas and breast cancer cells invariably express the activating transcription factor 5 (ATF5) and that loss of function of ATF5 caused massive apoptotic death of all cancer cell lines tested. ATF5 expression and function in pancreatic cancer cells have not been investigated. Materials and Methods: Quantitative real-time/reverse transcription-polymerase chain reaction (QRT/RT-PCR), western blotting (WB), immunohistochemistry (1HC) and promoter reporter assay were used for gene expression analysis. MTT [3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay and FACS (fluorescence-activated cell sorting) analysis were used to monitor cell viabilitylapoptosis. Results: ATF5 is highly expressed in pancreatic cancer cells as compared with non-tumor tissues. Both paclitaxel treatment and loss of function of ATF5 elicited apoptosis of SW1990 cells. Interference with ATF5 function in SW1990 cells resulted in down-regulation of BCL-2 and up-regulation of BAX, resulting in enhanced sensitivity to apoptosis induced by paclitaxel treatment. Conclusion: ATF5 is highly expressed in pancreatic cancer cells. Targeting ATF5 significantly enhances paclitaxel-induced apoptosis in human pancreatic cancer cells. ATF5 could be an important therapeutic target far pancreatic cancer treatment.

Human cytomegalovirus (HCMV) is a widespread pathogen, the most common congenital viral infection, and the leading cause of infant hepatitis syndrome. In this study, serum samples were collected from 20 HCMV‐infected infants with hepatitis and 25 controls. Of the 25 infants in the control group, 5 were infected with HCMV but without hepatitis, 10 had hepatitis but no HCMV infection, and 10 were healthy. Proteomic expression in the serum was detected by WCX2 chips and surface‐enhanced laser desorption/ionization time‐of‐flight mass spectrometry (SELDI‐TOF‐MS), to identify serum protein biomarkers in infants with hepatitis syndrome resulting from HCMV. Fifteen protein peaks were distinctly different among the four groups in the mass range from 2,000 to 20,000 Da. Of these 15 peaks, 4 at 4,349.8, 5,808.7, 7,935.6, and 8,885.9 Da were significantly different between the congenital HCMV‐infected infants with hepatitis and the controls. Five peaks were distinctly up‐regulated in the infants with HCMV infection (3,266.8, 5,638.5, 5,909.1, 7,771.4, and 15,835.6 Da) compared to those without HCMV infection. Two proteins at 4,600.1 and 5,704.3 were up‐regulated in infants with HMCV infection but no hepatitis. Four protein peaks were markedly different (7,567.0, 13,744.8, 15,100.7, and 15,915.0 Da) between the infants with hepatitis and the other controls. Comparison of the differentially expressed proteins' properties with those available on an international database suggest that specific serum proteins such as the augmenter of liver regeneration, pre‐albumin, and haptoglobin closely related to liver function, and cytokines such as beta‐defensins 31 and 8, and macrophage‐derived chemokine, among others, are involved in HMCV infection and the pathogenesis of HMCV‐induced hepatitis in infants. J. Med. Virol. 79:1500–1505, 2007. © Wiley‐Liss, Inc.

To detect differential protein expression in malignant and normal liver cell lines in vitro using the SELDI ProteinChip platform, for investigating the pathogenesis of liver cancer.

The cDNA encoding a protease of Perinereis aibuhitensis Grube (PPA) was cloned. The deduced amino acid sequence analysis showed that the protein had