AIM： To determine whether midkine （M/O and its truncated form （tMK） contribute to gastric tumorigenesis using in vitro and in vivo models. METHODS： Human MK and tMt（ plasmids were constructed and expressed in BG...AIM： To determine whether midkine （M/O and its truncated form （tMK） contribute to gastric tumorigenesis using in vitro and in vivo models. METHODS： Human MK and tMt（ plasmids were constructed and expressed in BGC823 （a gastric adenocarcinoma cell line） to investigate the effect of over-expressed MK or tMK on cell growth and turmorigenesis in nude mice. RESULTS： The growth of MK-transfected or tMK- transfected cells was significantly increased compared with that of the control cells, and tMK-transfected cells grew more rapidly than MK-transfected cells. The number of colony formation of the cells transfected with MK or tMK gene was larger than the control 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 than in control animals that were injected with cells without the transfection of either genes. CONCLUSION： Over-expressed MK or tMtC can promote human gastric cancer cell growth in vitro and in vivo, and bMK has greater effect than MK. tMK may be a more promising gene therapeutic target compared with MK for treatment of malignant tumors.展开更多
基金Supported by The Scientific Research Fund of Graduate School of Nanjing University, the Fund for Key Program of Ministry of Education, No. 02111the 985-Ⅱ Program of Nanjing University
文摘AIM： To determine whether midkine （M/O and its truncated form （tMK） contribute to gastric tumorigenesis using in vitro and in vivo models. METHODS： Human MK and tMt（ plasmids were constructed and expressed in BGC823 （a gastric adenocarcinoma cell line） to investigate the effect of over-expressed MK or tMK on cell growth and turmorigenesis in nude mice. RESULTS： The growth of MK-transfected or tMK- transfected cells was significantly increased compared with that of the control cells, and tMK-transfected cells grew more rapidly than MK-transfected cells. The number of colony formation of the cells transfected with MK or tMK gene was larger than the control 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 than in control animals that were injected with cells without the transfection of either genes. CONCLUSION： Over-expressed MK or tMtC can promote human gastric cancer cell growth in vitro and in vivo, and bMK has greater effect than MK. tMK may be a more promising gene therapeutic target compared with MK for treatment of malignant tumors.
