A Promising Tumor Gene Therapeutic Target: TMK

Main Category: Cancer / Oncology
Also Included In: GastroIntestinal / Gastroenterology;  Genetics;  Biology / Biochemistry
Article Date: 21 May 2008 - 4:00 PDT

email to a friend   printer friendly   view / write opinions   rate article

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

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.

----------------------------
Article adapted by Medical News Today from original press release.
----------------------------

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

Correspondence to: Ya-Yi Hou, Immunology and Reproductive Biology Lab, Medical School and State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing, Jiangsu Province, China.

About World Journal of Gastroenterology

World Journal of Gastroenterology (WJG), a leading international journal in gastroenterology and hepatology, has established a reputation for publishing first class research on esophageal cancer, gastric cancer, liver cancer, viral hepatitis, colorectal cancer, and H pylori infection for providing a forum for both clinicians and scientists. WJG has been indexed and abstracted in Current Contents/Clinical Medicine, Science Citation Index Expanded (also known as SciSearch) and Journal Citation Reports/Science Edition, Index Medicus, MEDLINE and PubMed, Chemical Abstracts, EMBASE/Excerpta Medica, Abstracts Journals, Nature Clinical Practice Gastroenterology and Hepatology, CAB Abstracts and Global Health. ISI JCR 2003-2000 IF: 3.318, 2.532, 1.445 and 0.993. WJG is a weekly journal published by WJG Press. The publication dates are the 7th, 14th, 21st, and 28th day of every month. The WJG is supported by The National Natural Science Foundation of China, No. 30224801 and No. 30424812, and was founded with the name of China National Journal of New Gastroenterology on October 1, 1995, and renamed WJG on January 25, 1998.

About The WJG Press

The WJG Press mainly publishes World Journal of Gastroenterology.

Source: Jing Zhu
World Journal of Gastroenterology