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【medical-news】一种很有前景的肿瘤治疗靶分子：
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. 本人已认领该文编译，48小时后若未提交译文，请其他战友自由认领 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.
由Ya-Yi Hou教授所领导的小组这项研究，以一份研究报告的形式刊登在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.
中期因子（MK） ，是一种肝素结合生长因子，其截断形式（tMK）在各种恶性肿瘤更高层度表达。MK和tMK的许多功能已经有报道。MK可以促进Wilms'肿瘤细胞增殖和肿瘤血管生成，抑制肿瘤细胞凋亡，诱导NIH3T3细胞的转化，并保护肝癌细胞避免TRAIL-途径介导的细胞凋亡。不过，一直没有MK和tMK对于胃癌的特征性效用的研究。
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.
在这项研究中，人类MK和tMK高表达质粒的构建和转染是用来研究;过度表达MK或tMK对BGC823（胃腺癌细胞系）的细胞生长和裸鼠体内肿瘤发生的影响。
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.
与对照组相比，MK转染的或tMK转染的细胞生长显著增长，并且tMK转染细胞的增长比MK转染的细胞增长更加迅速。MK转染或tMK转染的细胞可视地接种在裸鼠体内，肿瘤可以更早被发现，在尺寸和重量上更大。
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.
进一步的研究还应该鉴别：中期因子或截断中期因子在人胃癌中的过度表达对同正常的人胃组织在分子水平上的不同。这将是MK或tMK对于肿瘤生长的研究必不可少的步骤。 编译：
由Ya-Yi Hou教授领导的小组开展的这项研究，以一份研究报告的形式刊登在the World Journal of Gastroenterology。
中期因子（MK），是一种肝素结合的生长因子，其截断形式（tMK）在各种恶性肿瘤更高度的表达。MK和tMK的许多功能已经有报道。MK可以促进Wilms'肿瘤细胞增殖和肿瘤血管生成，抑制肿瘤细胞凋亡，诱导NIH3T3细胞的转化，并保护肝癌细胞避免TRAIL-途径介导的细胞凋亡。不过，一直没有MK和tMK对于胃癌的特征性效用的研究。
在这项研究中，人类MK和tMK高表达质粒的构建和转染是用来研究;过度表达MK或tMK对BGC823（胃腺癌细胞系）的细胞生长和裸鼠体内肿瘤发生的影响。
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作者:admin@医学,生命科学 2010-11-06 05:11
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