摘要
目的观察缺氧诱导因子-1α(HIF-1α)对HepG2细胞生长及凋亡相关蛋白的影响,并探讨其意义。方法将H1F-1α转染入人肝癌细胞HepG2中,观察HepG2细胞生长。建立人肝癌裸鼠模型,随机将其分为两组：对照组(A组,10只),HIF-1α转染细胞组(B组,10只)。1个月后,切除瘤灶、称瘤重、计算促瘤率。标本用Western blot检测HIF-1α、凋亡相关蛋白Survivin、bcl-2和Caspase-3的表达。结果HIF-1α转染HepG2细胞后,细胞生长速率加快。转染HIF-α的裸鼠肿瘤生长较对照组快,A组、B组的瘤重分别为(3．51±0．33)、(4．64±0．40)g,促瘤率为32%。B组HIF-1α、Survivin和bcl-2的蛋白水平明显高于A组,但Caspase-3的水平则低于A组。结论转染HIF-1α体内、外均可促进肝癌HepG2细胞的生长,其机制除促进血管生成外,还可能与其能抑制凋亡有关。
Objective To study the effects of hypoxia-inducible factor-lalpha （HIF-1α） on the expression of apoptosis related proteins and HepG2 cells growth. Methods To observe the growth rate of HepG2 cells after HIF-1α transfected. HepG2 cells （1×10^6/mouse） were inoculated subcutaneously into 20 nude mice, which were randomly divided into two groups：the control group （group A, n = 10）, the HIF-1α transfected group （group B, n = 10）. The weights of subcutaneous tumor were detected. The expressions of HIF-1α,survivin,bcl-2 and caspase 3 were analyzed by Western blot. Results The growth rates of HIF-1α transfected hepatic cancer cells were significantly increased, and more importantly, HIF-1α was able to enhance hepatic cancer growth in nude mice （P 〈 0.05）. The expressions of HIF-1α,survivin and bcl-2 in group B were increased significantly than that of group A,the expression of caspase 3 in group B was decreased significantly than that of group A. Conclusion HIF-1α could increase hepatic cancer cells HepG2 growth in vitro and in vivo and its mechanism may be due to the fact that It can inhibit apoptosis.
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
2006年第10期1203-1205,共3页
Chinese Journal of Experimental Surgery
