Liu F, Wu J Z, Li F, Li Y, Li J
Department of Oral Biology, College of Stomatology, Fourth Military Medical University, Xi'an,Shaanxi Province, China.
Cytotherapy. 2008;10(7):753-8. doi: 10.1080/14653240802357049.
The fragile histidine triad (FHIT) gene is abnormally expressed in many kinds of tumors and plays an important role in tumor development. However, the function of the FHIT gene in muco-epidermoid carcinoma (MEC) is still unknown. This study aimed to investigate the effect of exogenous FHIT gene on the biologic properties of MEC cells.
Wild-type FHIT gene was transferred into MEC-1 cells. The in vitro proliferation, clone formation ability and apoptosis of FHIT-transfected MEC-1 cells (MEC-FHITc4) were examined by cell counting, clonal forming assay, immunochemical staining, histochemical staining, flow cytometry analysis and transmission electron microscopy. The tumorigenicity of MEC-FHITc4 cells was observed by in vivo study in nude mice.
In vitro study showed that the population doubling times of MEC-1 and MEC-FHITc4 cells were 21.03 h and 26.86 h, respectively. FHIT gene transfer reduced the percentage of cells in cell cycle S phase (3.8%) and kept more cells in the G(1) phase (62.4%). Additionally, the clonal forming rates of MEC-1 and MEC-FHITc4 were 17.9+/-0.87% and 12.3+/-0.02%, respectively. In a 4-week tumor growth study in nude mice, FHIT transfection suppressed the tumor growth by 70.1+/-0.38%. Interestingly, MEC-FHITc4 cells were stained more strongly with Alician Blue and Periodic Schiffs than control cells.
The FHIT gene might function to inhibit the proliferation and tumorigenicity of MEC-1 cells, and to induce the differentiation of MEC-1 cells, in vitro and in vivo.
脆性组氨酸三联体（FHIT）基因在多种肿瘤中异常表达，在肿瘤发生发展中起重要作用。然而，FHIT基因在黏液表皮样癌（MEC）中的功能仍不清楚。本研究旨在探讨外源性FHIT基因对MEC细胞生物学特性的影响。
将野生型FHIT基因转入MEC-1细胞。通过细胞计数、克隆形成试验、免疫化学染色、组织化学染色、流式细胞术分析和透射电子显微镜检查，检测转染FHIT基因的MEC-1细胞（MEC-FHITc4）的体外增殖、克隆形成能力和凋亡情况。通过裸鼠体内研究观察MEC-FHITc4细胞的致瘤性。
体外研究显示，MEC-1细胞和MEC-FHITc4细胞的群体倍增时间分别为21.03小时和26.86小时。FHIT基因转移降低了细胞周期S期的细胞百分比（3.8%），使更多细胞处于G(1)期（62.4%）。此外，MEC-1细胞和MEC-FHITc4细胞的克隆形成率分别为17.9±0.87%和12.3±0.02%。在裸鼠为期4周的肿瘤生长研究中，FHIT转染使肿瘤生长抑制了70.1±0.38%。有趣的是，与对照细胞相比，MEC-FHITc4细胞对阿利新蓝和过碘酸希夫反应的染色更强。
FHIT基因可能在体外和体内发挥作用，抑制MEC-1细胞的增殖和致瘤性，并诱导MEC-1细胞分化。
