Inability to induce the alteration of tumorigenicity and chemosensitivity of p53-null human pancreatic carcinoma cells after the transduction of wild-type p53 gene.
Inability to induce the alteration of tumorigenicity and chemosensitivity of p53-null human pancreatic carcinoma cells after the transduction of wild-type p53 gene.
复制标题
转导野生型p53基因后，无法诱导p53缺失的人胰腺癌细胞的致瘤性和化疗敏感性改变。
作者：
Masaki Kimura;Masatoshi Tagawa;K. Takenaga;Taketo Yamaguchi;H. Saisho;Akira Nakagawara;Shigeru Sakiyama
我们研究了通过将野生型p53基因转导到p53缺失的人胰腺癌细胞（AsPC-1）中来表达p53的治疗益处。转染p53基因的AsPC-1细胞中可见p21 WAF 1/CIP 1蛋白的诱导表达，表明整合的p53基因具有正常的功能。然而，转导细胞的体外细胞生长与亲本细胞没有差异，并且转导细胞接种到裸鼠中的肿瘤生长与野生型细胞相比没有变化。此外，在体外敏感性的4种不同的抗癌药物，包括顺铂，依托泊苷，5-氟尿嘧啶和紫杉醇，不调制野生型p53基因的表达。因此，本文提供的数据表明，野生型p53基因在p53-null肿瘤细胞中的表达并不一致地产生先前报道的治疗效果。
We investigated the therapeutic benefits of p53 expression by the transduction of wild-type p53 gene into p53-null human pancreatic carcinoma cells (AsPC-1). Induction of p21WAF1/CIP1 protein was observed in p53 gene-transduced AsPC-1 cells, showing the proper function of integrated p53 gene. However, the cell growth in vitro of transduced cells was not different from that of parent cells, and the tumor growth of transduced cells inoculated into nude mice was unchanged compared with that of wild-type cells. Moreover, the in vitro sensitivity to 4 different kinds of anticancer agents including cisplatin, etoposide, 5-fluorouracil and paclitaxel, was not modulated by the expression of wild-type p53 gene. Thus, the data presented here suggest that the expression of wild-type p53 gene in p53-null tumor cells does not consistently produce the therapeutic effects previously reported.