Hsu S L, Lin H M, Chou C K
Department of Education and Research, Taichung Veterans General Hospital, Taiwan, Republic of China.
Cancer Lett. 1996 Jan 19;99(1):79-85. doi: 10.1016/0304-3835(95)04040-4.
We cultured human hepatoma Hep3B cells in the presence of RA (10(-5) M) for 30 days; the expression of both alpha-fetoprotein and hepatitis B virus surface antigen were suppressed over 70% at the transcriptional level by RA treatment. The doubling time of RA treated Hep3B cells was slightly different from the control cells when they were cultured in 5% fetal calf serum/DMEM medium. However, cultured under serum-free conditions, the control Hep3B cells still grow, but the RA treated cells could not attach to the substratum of the culture plate and stopped growing. In vivo assay indicated that RA treatment completely suppressed the tumorigenicity of Hep3B cells in nude mice.
我们在视黄酸(RA,10⁻⁵ M)存在的情况下培养人肝癌Hep3B细胞30天;经RA处理后,甲胎蛋白和乙型肝炎病毒表面抗原在转录水平的表达均被抑制超过70%。当在5%胎牛血清/杜氏改良 Eagle 培养基中培养时,经RA处理的Hep3B细胞的倍增时间与对照细胞略有不同。然而,在无血清条件下培养时,对照Hep3B细胞仍能生长,但经RA处理的细胞无法附着于培养板的基质上并停止生长。体内试验表明,RA处理完全抑制了Hep3B细胞在裸鼠中的致瘤性。