A promising tumor gene therapeutic target: tMK (5/23/2008)

This study, performed by a team led by Professor Ya-Yi Hou, is described in a research article to be published in the World Journal of Gastroenterology on March 28, 2008.

Midkine (MK), a heparin-binding growth factor, and its truncated form (tMK) are expressed at higher levels in various malignant tumors. Many functions of MK and tMK have been reported. MK can promote Wilms' tumor cell proliferation and tumor angiogenesis, inhibit tumor cells apoptosis, induce transformation of NIH3T3 cells, and protect hepatocellular carcinoma cells against TRAIL-mediated apoptosis. However, there has been no research on the effect of MK and tMK on the characteristics of gastric carcinoma.

In this study, human MK and tMK highly expressed plasmids were constructed and transfection assay was used to study the effect of over-expressed MK or tMK on cell growth of BGC823 (gastric adenocarcinoma cell line) and tumorigenesis in nude mice.

The growth of MK-transfected or tMK-transfected cells was significantly promoted compared with the control cells, and tMK- transfected cells grew more rapidly than MK-transfected cells. In nude mice injected with MK-transfected or tMK-transfected cells visible, tumor was observed earlier and the tumor tissues were larger in size and weight.

Further research should describe the differences between the midkine or truncated midkine overexpressed human gastric cancer and normal human gastric tissue at a molecular level. This would be essential in studying the effect of MK or tMK on tumor growth.

Reference: Wang QL, Wang H, Zhao SL, Huang YH, Hou YY. Overexpressed and truncated Midkines promote proliferation of BGC823 cells in vitro and tumor growth in vivo. World J Gastroenterol 2008; 14(12): 1858-1865 http://www.wjgnet.com/1007-9327/14/1858.asp

Note: This story has been adapted from a news release issued by the World Journal of Gastroenterology

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