Su Zhang

Renji Hospital, Shanghai, Shanghai Shi, China

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Publications (2)3.65 Total impact

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    ABSTRACT: Pancreatic cancer typically has an unfavourable prognosis due to late diagnosis and a lack of therapeutic options. Thus, it is important to better understand its pathological mechanism and to develop more effective treatments for the disease. Human chromosome 20q13 has long been suspected to harbour oncogenes involved in pancreatic cancer and other tumours. In this study, we found that eEF1A2, a gene located in 20q13, was significantly upregulated in pancreatic cancer. Little or no expression of eEF1A2 was detected in normal human pancreatic and chronic pancreatitis tissues, whereas increased eEF1A2 expression occurred in 83% of the pancreatic cancers we studied. Furthermore, using in vitro and in vivo model systems, we found that overexpression of eEF1A2 promoted cell growth, survival, and invasion in pancreatic cancer. Our data thus suggest that eEF1A2 might play an important role in pancreatic carcinogenesis, possibly by acting as a tumour oncogene.
    Biochemical and Biophysical Research Communications 02/2009; 380(1):11-6. DOI:10.1016/j.bbrc.2008.12.171 · 2.30 Impact Factor
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    ABSTRACT: Pancreatic carcinoma is one of the most aggressive malignancies and carries the most dismal prognoses of all cancers. A better understanding of the genes involving in tumor development may allow us to tackle this rapidly progressive disease. The Net gene belongs to the ternary complex transcription factor (TCF) family and is regulated by the Ras/mitogen-activated protein kinase-signaling pathway. Under basal conditions, Net shows strong repressing function on transcription of proto-oncogene gene c-fos. Moreover, the lower expression of Net has been noted in some carcinoma cells, such as cervical cancer. To study the effect of Net on c-fos expression and its potential role in the growth of pancreatic carcinoma, we developed a recombinant plasmid, a pEGFP-N1-Net, which codes for Net-EGFP fusion proteins, and stably transfected it into BxPC-3 human pancreatic carcinoma cells. Using stable transformants, we were able to show that overexpression of Net decreased the expression of c-fos and inhibited pancreatic cancer cell proliferation. Cell cycle analysis demonstrated that Net overexpression inhibited cell cycle progression. These findings suggested that loss of Net repression could augment c-fos expression and further trigger neoplastic cell proliferation, which was involved in the pathogenesis of pancreatic cancer. Therefore, Net might be a potential target for the treatment of c-fos-positive pancreatic cancer.
    The Tohoku Journal of Experimental Medicine 11/2008; 216(2):139-47. DOI:10.1620/tjem.216.139 · 1.35 Impact Factor