ABSTRACT: To explore the co-operative inhibitory effect of antisense VEGF gene and endostatin gene transfection on tumor angiogenesis, tumor growth and metastasis of lung cancer.
Antisense VEGF₁₂₁ cDNA was transfected into PG cells(PG-AS-VEGF) by lipofectin. After PG-AS-VEGF cells were xenografted to nude mice, PsectagA-endostatin gene was transfected into nude mice by electric pulse mediation. The MVDs in tumors and tumor biological characteristics were observed.
(1)The MVD in PG-AS-VEGF tumor in nude mice was significantly lower than that in PG-vector tumor (PG-AS-VEGF and PG-vector: 40.67±9.35 and 58.34±10.52, respectively) in nude mice. (2)There was no significant difference between the PG-vector tumor and PG-AS-VEGF tumor in early stage of the tumor growth in vivo. However, PG-AS-VEGF tumor grew significantly more slowly than PG-vector tumor after 18 days (P<0.05). (3)PG-AS-VEGF tumor could lead to regional and/or distant lymph node metastases (16.7%, 2/12), which was much more infrequent than that in PG-vector group (50%, 6/12). (4) PG-AS-VEGF tumor growth was remarkably inhibited by endostatin gene transfected at site of the tumor inoculation as compared with the control group in nude mice (P<0.05). (5)The PG-AS-VEGF tumors transfected with the endostatin gene at site of the tumor inoculation(AST) could also produce much lower regional and/or distant lymph node metastases rate (12.5%, 1/8) than that in the PG-AS-VEGF tumor transfected with the PsectagA vector (ASP)(75%, 6/8).
Endostatin gene transfection could cooperatively inhibit the growth and spontaneous lymph node metastasis of antisense VEGF gene transfected PG cells in nude mice.
Zhongguo fei ai za zhi = Chinese journal of lung cancer 04/2001; 4(2):83-7.