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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 observe the effect of hypoxia inducible factor-1α (HIF-1α) on the growth and apoptosis-related proteins in HepG2 cells and to explore its significance. Methods H1F-1α was transfected into human hepatoma HepG2 cells to observe the growth of HepG2 cells. The human hepatocellular carcinoma model was established and divided into two groups at random: control group (group A, n = 10) and HIF-1α transfected group (group B, n = 10). One month later, the tumor was excised and weighed to calculate the tumor-promoting rate. Western blot was used to detect the expression of HIF-1α, apoptosis-related proteins Survivin, bcl-2 and Caspase-3. Results After HepG2 cells were transfected with HIF-1α, the cell growth rate was accelerated. The tumor growth of HIF-α-bearing nude mice was faster than that of the control group. The tumor weights of group A and group B were (3.51 ± 0.33) and (4.64 ± 0.40) g, respectively, 32%. The protein level of HIF-1α, Survivin and bcl-2 in group B was significantly higher than that in group A, but the level of Caspase-3 was lower than that in group A. Conclusion Transfection of HIF-1α in vitro and in vivo can both promote the growth of HepG2 hepatocellular carcinoma cells. The mechanism may be related to the inhibition of apoptosis by promoting the angiogenesis.