Changes in Bcl-2 and Bax expression in rat tongue during 4-nitroquinoline 1-oxide-induced carcinogenesis
Changes in Bcl-2 and Bax expression in rat tongue during 4-nitroquinoline 1-oxide-induced carcinogenesis
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DOI：
10.1177/00220345990780061101
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发表时间：
1999-06-01
影响因子：
7.6
通讯作者：
Nishimura, A
中科院分区：
文献类型：
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作者：
Nishimura, A
Bax被认为是细胞凋亡的主要效应因子。Bax与Bcl-2形成同源二聚体和异源二聚体。在活性细胞死亡中，Bax-Bax二聚体的功能被Bcl-2异源二聚体拮抗。因此，Bcl-2和Bax的比例应该控制细胞对诱导凋亡性细胞死亡的那些刺激的易感性。在许多癌中已经显示出凋亡变化的增加。本研究采用4-硝基喹啉1-氧化物（4 NQO）诱发的小鼠肝癌模型，用免疫组化方法检测了癌转化过程中Bcl-2和Bax表达的变化。将动物分成7组，每组10只大鼠，并给予59 ppm 4 NQO溶液作为饮用水，持续4、8、12、16、20或24周。10只动物用作对照。Bcl-2-和Bcl-2-阳性细胞的数量逐渐增加，相应的实验性癌变的进展。Bcl-2和Bax的表达在对照组和4周治疗组之间（p < 0.01），以及在对照组和8周治疗组之间（p < 0.05）分别显示出统计学显著性差异。这两种蛋白质的水平仍然很高的上皮细胞发育不良的变化期间后。结论：Bcl-2和Bax参与了4 NQO诱导的肿瘤的发生发展。
Bax is considered as a main effector of apoptosis. Bax forms homodimers and also heterodimers with Bcl-2. The function of the Bax-Bax dimer in active cell death is antagonized by Bax-Bcl-2 heterodimers. Thus, the ratio of Bcl-2 and Bax should control the susceptibility of cells to those stimuli that induce apoptotic cell death. An increase in apoptotic change has been shown in many carcinomas. In the present study, the changes in Bcl-2 and Bax expression in the tissue during carcinogenic transformation were examined immunohistochemically by means of the 4-nitroquinoline 1-oxide (4NQO)-induced carcinoma model. Animals were divided into 7 groups of 10 rats each, and given 59 ppm 4NQO solution as drinking water for 4, 8, 12, 16, 20, or 24 weeks. Ten animals were used as controls. Gradual increases in the numbers of Bcl-2- and Bax-positive cells were shown corresponding to the progression of experimental carcinogenesis. Statistically significant differences in Bcl-2 and Bax expression were demonstrated between control and four-week treatment groups (p < 0.01), and between control and eight-week treatment groups (p < 0.05), respectively. Levels of both proteins remained high after the period of dysplastic change of the epithelium. In conclusion, Bcl-2 and Bax are involved in the progression of 4NQO-induced carcinoma.