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目的观察携带人野生型ｐ５３、ＧＭ－ＣＳＦ和Ｂ７－１基因的重组腺病毒载体（ＢＢ－１０２）转染ＢＥＬ－７４０２、ＨＬＥ及ＨｕＨ－７肝癌细胞后ｐ５３基因的表达，以及诱导肝癌细胞凋亡，影响肝癌细胞的增殖。方法ＢＢ－１０２以ＭＯＩ为５０ｐｆｕ／细胞 感染肝癌细胞系ＢＥＬ－７４０２（ｐ５３基因为野生型）、ＨＬＥ及ＨｕＨ－７（ｐ５３基因为突变型）。免疫组织化学祛检测ＢＢ－１０２携带的ｐ５３基因的表达，ＴｄＴ法原位检测肝癌细胞的凋亡。结果ＢＢ－１０２携带的ｐ５３基因能在转染了 ＢＢ－１０２的肝癌细胞中高效表达。转染 ＢＢ－１０２后肝癌细胞生长明显受到抑制；染毒后第 ４－ １０ ｄ期间， ＢＥＬ－７４０２、 ＨＬＥ及 ＨｕＨ－７三株肝癌细胞的平均受抑率分别为 ５８．５％、 ８１．５％及７１．１％，其中对 ｐ５３基因突变的肝癌细胞的抑制程度要大于对ｐ５３基因为野生型肝癌细胞的抑制程度。转染ＢＢ－１０２还能诱导肝癌细胞的凋亡。结论ＢＢ－１０２通过其介导ｐ５３基因的表达抑制肝癌细胞的增殖，这为ＢＢ－１０２应用于肝癌的基因治疗提供实验依据。
Objective To observe the expression of p53 gene in BEL-7402, HLE and HuH-7 liver cancer cells transfected with human wild-type p53, GM-CSF and B7-1 gene recombinant adenovirus vector (BB-102), and to induce apoptosis of hepatocellular carcinoma cells. It will affect the proliferation of liver cancer cells. Methods BB-102 was infected with the hepatoma cell line BEL-7402 (p53 gene was wild type), HLE and HuH-7 (p53 gene was mutant) at an MOI of 50 pfu/cell. The expression of p53 gene carried by BB-102 was detected by immunohistochemistry, and the apoptosis of hepatoma cells was detected by TdT method in situ. Results The p53 gene carried by BB-102 was highly expressed in hepatoma cells transfected with BB-102. The growth of hepatoma cells was significantly inhibited after transfected with BB-102. During the 4th to 10th day after exposure, the average inhibition rates of BEL-7402, HLE and HuH-7 hepatoma cells were 58.5% and 81.8%, respectively. 5% and 71.1%, of which the degree of inhibition of p53 gene mutation in hepatoma cells was greater than that of p53 gene in wild-type hepatoma cells. Transfection of BB-102 can also induce apoptosis of hepatoma cells. Conclusions BB-102 inhibits the proliferation of hepatocellular carcinoma cells by mediating the expression of p53 gene, which provides an experimental basis for gene therapy of BB-102 in hepatocellular carcinoma.