华西口腔医学杂志

• 基础研究 • 上一篇    下一篇

脆性组氨酸三聚体基因对黏液表皮样癌细胞生长抑制作用的研究

刘峰1, 吴军正2, 李峰2, 李焰2, 李洁2   

  1. 1.第四军医大学口腔医院口腔材料学教研室; 2.口腔生物学教研室, 陕西西安710032
  • 收稿日期:2008-06-25 修回日期:2008-06-25 出版日期:2008-06-20 发布日期:2008-06-20
  • 通讯作者: 刘峰,Tel:029- 84776181
  • 作者简介:刘峰(1965-),女,陕西人,副教授,博士

The inhibition of fr agile histidine tr iad gene on the prolifer ation and tumor igenicity of mucoepidermoid car cinoma cells

LIU Feng1, WU Jun- zheng2, LI Feng2, LI Yan2, LI Jie2   

  1. 1. Dept. of Dental Materials, College  of Stomatology, The Fourth Military Medical University, Xi′an 710032, China;2. Dept. of Oral Biology, College of Stomatology, The Fourth Military Medical University, Xi′an 710032, China
  • Received:2008-06-25 Revised:2008-06-25 Online:2008-06-20 Published:2008-06-20
  • Contact: LIU Feng,Tel:029- 84776181

摘要:

目的探讨外源性脆性组氨酸三聚体(FHIT)基因的转入对黏液表皮样癌细胞增殖和生长的抑制作用。方法通过透射电镜、流式细胞仪测试、免疫组化染色及肿瘤细胞裸鼠移植实验,将转入外源性FHIT基因前后的黏液表皮样癌MEC- 1细胞的体外生物学活性和体内成瘤能力进行比较。结果外源性FHIT基因转入黏液表皮样癌MEC- 1细胞后,S期细胞显著减少,G1期细胞增多;细胞倍增时间从(21.03±0.41)h延长为(26.86±0.71)h;软琼脂克隆形成率显著降低;细胞发生退行性改变和出现凋亡早期表现。FHIT基因转染后细胞间质黏液增多,说明细胞向黏液细胞分化。结论外源性FHIT基因能够抑制黏液表皮样癌MEC- 1细胞的生长和MEC- 1细胞在体内的成瘤活性,而且可以提高MEC- 1癌细胞的分化程度。

关键词: 脆性组氨酸三聚体, 基因转染, 黏液表皮样癌, 成瘤性

Abstract:

Objective To investigate the suppression effect of exogenous fragile histidine triad(FHIT) gene on biological property of MEC- 1 cells. Methods In order to study the FHIT function in MEC- 1 cells, wild- type FHITgene was transferred into mucoepidermoid carcinoma MEC- 1 cells. The proliferation and kinetics, cell cycle, clonal forming rate, and apoptosis of MEC- 1 cells, before and after FHIT gene transfection in vitro, and tumor loci formed on mice after injection of transferred MEC- 1 cells in vivo were observed by immunochemical staining, flow cytometry analysis, and so on. Results It can be seen that exogenous FHIT gene transfer could significantly inhibit the proliferation and reduce the kinetics of MEC- 1 cells in vitro, prolong DT from(21.03±0.41)h to(26.86±0.71)h, and also keep less cells in cell cycle phase S, whilst more cells in phase G1, Additionally, the exogenous FHIT was found to be able to remarkably suppress MEC- 1 cells of forming tumor loci in nude mice by lessen tumor weight, and promote higher differentiation of MEC- 1 cells to be mucous cells. Conclusion Exogenous FHIT gene could suppress the proliferation, tumorigenicity and improve the differentiation of MEC- 1 cells, in vitro and in vivo.

Key words: fragile histidine triad, gene transfer, mucoepidermoid carcinoma, tumorigenicity