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目的探讨在体外常氧条件下,诱导表达缺氧诱导因子1α(HIF-1α)对肝癌细胞(HepG2)增殖及侵袭能力的影响。方法利用 Tet-on 基因调控系统构建能诱导表达 HIF-1α的HepG2~(Tet-on-HIF-1α)细胞系;常氧条件下,噻唑兰法检测 HIF-1α对细胞增殖、黏附能力的影响,Transwell 法检测其对 HepG2细胞侵袭能力的影响。结果常氧条件下,强力霉素(1μg/ml)可诱导HepG2~(Tet-on-Hlf-1α)细胞 HIF-1αmRNA 和蛋白表达增加;增殖实验中,Dox(+)组与 Dox(-)组各时段吸光度 A_(490nm)值无差异(P>0.05);黏附实验中,Dox(+)组的 A_(490nm)值明显高于 Dox(-)组(P=0.008);Dox(+)组侵袭细胞数[(37.611±8.424)个]明显高于 Dox(-)组[(25.333±8.117)个](P<0.01)。结论 Tet-on 基因调控系统可上调 HIF-1α mRNA 的转录并增加其蛋白的表达;常氧条件下,HIF-1α不影响 HepG2细胞的增殖,但明显增加其黏附和侵袭能力。
Objective To investigate the effect of hypoxia inducible factor 1α (HIF-1α) on the proliferation and invasion of HepG2 cells under normoxia in vitro. Methods The Tet-on-HIF-1α cell line was induced by Tet-on gene regulation system. The effect of HIF-1α on the proliferation and adhesion of HIF-1α was detected by MTT assay under normoxia Transwell assay was used to detect the invasion ability of HepG2 cells. Results Under normoxic conditions, doxorubicin (1μg / ml) induced an increase in HIF-1αmRNA and protein expression in HepG2 Tet-on-Hlf-1αcells. In proliferation experiments, Dox (+ The values of A_ (490nm) in Dox (+) group were significantly higher than those in Dox (-) group (P = 0.008); Dox (+) The number of invasive cells in group [(37.611 ± 8.424)] was significantly higher than that in Dox (-) group [(25.333 ± 8.117)] (P <0.01). Conclusions Tet-on gene regulatory system can up-regulate the transcription of HIF-1α mRNA and increase the expression of HIF-1α mRNA. Under normoxic condition, HIF-1α does not affect the proliferation of HepG2 cells, but significantly increases its adhesion and invasion ability.