| Colorectal cancer is one of the most common malignant tumors in our country.Themorbidity and mortality of colorectal cancer have increased yearly. Further research on etiology and pathology of colorectal cancer have been undertaken in recent years It was certain that occurrence of colorectal cancer was the result of interaction between hereditary and environmental factors, involved of activation of proto- oncogene and mutation of tumor suppressor genes,etc Comprehensive treatment model has been suggested on the management of colorectal cancer remedy, including operation, radiotherapy, chemotherapy, immunotherapy,gene therapy,etc The results are the increase of survival rate and improvement of the quality of life Gene therapy is a complete new in biotherapy,which is the introducing of genetic material into cells for therapeutic purposes. For colorectal cancer, there are suicide gene therapy(HSV-TK/GC"V system> CD/5-FC system), gene therapy about oncogene and tumor suppressor gene, immuno-gene therapy, anti-VEGF gene therapyTumor necrosis factor-related apoptosis-inducing ligand(TRAIL), a new member of the TNF family. It is a promising agent for tumor gene therapy because of its selective cytotoxic effect. TRAIL appears to induce cyto-apoptosis in tumongenic or transformed cells or virus infected cellsbut not in normal cells There are five TRAIL receptors:DR4, DR5 x DcRl > DcR2. OPG (Osteoprotegerin) ?Both member-bound TRAIL and solube TRAIL induce apoptosis rapidly via interaction with receptors DR4, DR5 But DcRl, DcR2 v OPG may compete with DR4 > DR5 for TRAIL binding ,thereby protecting normal cells from the cytotoxic effect. DcRl, lack of death domain and DcR2,with a truncated death domain are not capable of inducing apoptosis, however by competing for TRAlL,they are capable of inhibiting TRAlL-induced apoptosis.In addition,it is important for tumor gene therapy that TRAIL may elicit bystander effects either through interaction of surface TRAIL molecules with receptors on neighboring cells or through the action of soluble TRAIL from the TRAIL-expressing cells. Recent studies showed that TRAIL induced apoptosis in a wide of tumor cell lines, not only in cultured cells,but also in mice bearing solid tumors.In this study a binary adenoviral vector system was used for expressing and transferring TRAIL gene, cytotoxic effects of TRAIL on colorectal cancer cell line HT29 were measured by retromicroscopex MTT method and flow cytometryMaterials and MethodsAdenoviral vectors Ad'GT-TRAIL^ AdGT-Bax, Ad/GT-LacZ and Ad/PGK-GV16 were presented by Dr.Fangbingliang (Department of Thoractic and Cardiovascular surgery, The University of Texas M.D.Anderson Cancer center) Human embryonal kidney cells transformed by-introducing sheared fragments of Ad5 DNA.293 cell maintained in our laboratory(Climcal research institute of Sir Run Run Shaw Hospital).Human colorectal cancer cell line HT29 honored got from Dr Cuijunhui(Zhejiang Uiiversity,Medical College) Cytotoxic effects of TRAIL on colorectal cancer cell line HT29 were measured by retromicroscope, MTT method and flow cytometry(Annexin V-PI Kit).The statistical analysis was achieved by SPSS10.0 software.Results and Discussion 1 All adenoviral vectors titer determined by optical absorbency at A260nm were 1 X1010partical/mlo2, When HT29 were transfected with Ad/GT-TRAIL x Ad/GT-Bax, obviously morphological changes of HT29 were found. And the changes were much more obviously when Ad/PGK-GV 16 was cultured together. However, when HT29 were transfected with Ad/GT-LacZ x Ad/GT-LacZ+ Ad/PGK-GV16, no significantly morphological changes were found.3 Cultured wim Ad/GT-TRAIL ^ Ad/GT-Bax > Ad/GT-LacZ ,HT29 was inhibited 54.3% x 29.2%and 12.1%. When Ad/PGK-GV 16 was added, the cell growth inhibition rates were 82.7%x 57.4% and 14.2% respectively. There were significant difference between TRAIL> Bax and LacZ x PBS treatment; Ad/GT-TRAIL and Ad/GT-TRAIL+ Ad/PGK-GV 16, Ad/GT-Bax and Ad/GT-Bax+ Ad/PGK-GV16 (p<005). There were significant difference between TRAIL...
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