CAJ | 학술논문

用不同浓度的肿瘤坏死因子α(TNF-α)诱导人肝癌细胞(HepG2细胞),结果表明TNF-α上调HepG2细胞蛋白酪氨磷酸酶1B(PTP-1B)的表达,激活NF-kB,并呈浓度依赖性,抑制NF-kB能阻断TNF-α对HepG2细胞PTP-1B的上调作用.提示TNF-α可能通过激活NF-kB从而诱导HepG2细胞PTP-1B表达的上调.
용불동농도적종류배사인자α(TNF-α)유도인간암세포(HepG2세포),결과표명TNF-α상조HepG2세포단백락안린산매1B(PTP-1B)적표체,격활NF-kB,병정농도의뢰성,억제NF-kB능조단TNF-α대HepG2세포PTP-1B적상조작용.제시TNF-α가능통과격활NF-kB종이유도HepG2세포PTP-1B표체적상조.
HepG2 ceils were treated with various concentrations of tumor necrosis factor-or (TNF-α) for 24 hours. RT-PCR and Western blot were used to measure protein tyrosine phosphatase-1 B(PTP-1B)expression, and luciferase reporter assay was used to detect NF-kB activity. The results showed that treatment of HepG2 cells with TNF-α for 24 hours led to upregulation of PTP-1B and NF-kB activity in a dose-dependent manner. Inhibition of NF-kB by PI)TC significantly attenuated TNF-α-induced PTP-IB expression in HepG2 cells. Thus, the transactivation of NF-kB seems to play an important role in the expression of PTP-1B in HepG2 cells induced by TNF-α.