Mei-ning Li1, Ge Huang, Li-ping Guo, Shih-hsin Lu. 1. Department of Etiology & Carcinogenesis, Cancer Institute & Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100021, China.
Abstract
OBJECTIVE: To investigate the inhibitory role of esophageal cancer related gene 2 (ECRG2) on proliferation of human esophageal cancer cell EC9706. METHODS: Recombinant plasmid pcDNA3.1-ECRG2 with ECRG2 open reading frame was constructed. The cells were transfected with either pcDNA3.1 or pcDNA3.1-ECRG2 using Lipofectamin 2000. The expression of ECRG2 protein was examined by Dot Blot analysis. The effects of ECRG2 on cell proliferation and malignant was analyzed by colony formation assay. The variation of P53 and P21 were detected in EC9706 cells with or without expression of ECRG2. RESULTS: The plasmid of pcDNA3.1-ECRG2 was successfully established. Colony formation activity of EC9706/pcDNA3.1-ECRG2 was 18% while that of the control cell was 55% in six well plate (P < 0.05). The activity of anchorage-independent proliferation of EC9706/pcDNA3.1-ECRG2 was lower than that of EC9706/pcDNA3.1 in soft agar. After transfected with pcDNA3.1-ECRG2, the expression of P53 and P21 were higher than control. CONCLUSION: ECRG2 can reduced the abilities of proliferation and of anchorage-independent proliferation of EC9706 cells which is through p53 pathway possibility.
OBJECTIVE: To investigate the inhibitory role of esophageal cancer related gene 2 (ECRG2) on proliferation of humanesophageal cancer cell EC9706. METHODS: Recombinant plasmid pcDNA3.1-ECRG2 with ECRG2 open reading frame was constructed. The cells were transfected with either pcDNA3.1 or pcDNA3.1-ECRG2 using Lipofectamin 2000. The expression of ECRG2 protein was examined by Dot Blot analysis. The effects of ECRG2 on cell proliferation and malignant was analyzed by colony formation assay. The variation of P53 and P21 were detected in EC9706 cells with or without expression of ECRG2. RESULTS: The plasmid of pcDNA3.1-ECRG2 was successfully established. Colony formation activity of EC9706/pcDNA3.1-ECRG2 was 18% while that of the control cell was 55% in six well plate (P < 0.05). The activity of anchorage-independent proliferation of EC9706/pcDNA3.1-ECRG2 was lower than that of EC9706/pcDNA3.1 in soft agar. After transfected with pcDNA3.1-ECRG2, the expression of P53 and P21 were higher than control. CONCLUSION:ECRG2 can reduced the abilities of proliferation and of anchorage-independent proliferation of EC9706 cells which is through p53 pathway possibility.