Wang B, Yan C, Wu Y, Gao H, Wang Q, Jin Y, Huang C, Zhang G, Fu S, Li P
Department of Medical Genetics, Harbin Medical University, Harbin, Heilongjiang 150086 P. R. China.
Zhonghua Yi Xue Yi Chuan Xue Za Zhi. 2001 Apr;18(2):128-31.
In order to investigate the suppression effect of tumor suppressor genes in lung adenocarcinoma.
p16 and p21 expression vectors were transfected into a pair of lung adenocarcinoma cell lines with different metastasis potentials: Anip973(high metastasis potential)and AGZY83-a (low metastasis potential). In the mean time, AGZY83-a, Anip973, AGZY83-ap16 and Anip973p16 were infected with recombinant adenovirus encoding wild- type p53 gene. The suppression effects of these genes were evaluated by cell growth curve, MTT, cloning efficiency assay, flow cytometric analysis and TUNEL technique.
Overexpression of p16 gene in Anip973 and AGZY83-a could only lengthen the G(1) phase while increased expression of p21 in both of the cell lines was associated with significant lengthening of G(1) phase, decreased proliferation potential and decreased cloning efficiency. High efficient expression of wild-type p53 gene in AGZY83-a, Anip973, Anip973p16 and AGZY83-ap16 inhibited the growth of these four kinds of lung cancer cells and killed the cells in the end. Apoptosis was detected in all the four kinds of cells. The suppression effect of p53 gene was higher in Anip973 and Anip973p16 than in AGZY83-a and AGZY83-ap16 while co-expression of p53 and p16 in this pair of cell lines inhibited the cells more efficiently as compared with the expression of p53 gene.
Increased expression of p21 gene suppressed the lung adenocarcinoma cells by G(1) arrest and the co-transfection of tumor suppressor genes p16 and p53 into the lung adenocarcinoma cell line proved more effective in lung cancer gene therapy.
探讨抑癌基因对肺腺癌的抑制作用。
将p16和p21表达载体转染至一对具有不同转移潜能的肺腺癌细胞系：Anip973（高转移潜能）和AGZY83-a（低转移潜能）。同时，用编码野生型p53基因的重组腺病毒感染AGZY83-a、Anip973、AGZY83-ap16和Anip973p16。通过细胞生长曲线、MTT、克隆效率测定、流式细胞术分析和TUNEL技术评估这些基因的抑制作用。
Anip973和AGZY83-a中p16基因的过表达仅延长G(1)期，而这两种细胞系中p21表达的增加均与G(1)期显著延长、增殖潜能降低和克隆效率降低有关。野生型p53基因在AGZY83-a、Anip973、Anip973p16和AGZY83-ap16中的高效表达抑制了这四种肺癌细胞的生长并最终杀死细胞。在所有四种细胞中均检测到凋亡。p53基因在Anip973和Anip973p16中的抑制作用高于AGZY83-a和AGZY83-ap16，而在这对细胞系中p53和p16的共表达与p53基因的表达相比更有效地抑制了细胞。
p21基因表达增加通过G(1)期阻滞抑制肺腺癌细胞，将抑癌基因p16和p53共转染至肺腺癌细胞系在肺癌基因治疗中证明更有效。
