Department of Hepatobiliary Surgery, No. 1 People's Hospital in Jining, Shandong Jining, China.
Eur Rev Med Pharmacol Sci. 2017 Jun;21(11):2604-2610.
To study the role of TGF-β1 in autophagy and invasion ability of human hepatic carcinoma HepG2 cells.
Cultured HepG2 cells were treated with different concentrations of TGF-β1 for 24 h. The protein expression levels of autophagy relative marker LC3 and Beclin1 were detected by Western blot. The effect of TGF-β1 on invasion ability of HepG2 cells was detected with transwell method.
The results demonstrated that TGF-β1 was able to activate autophagy of HepG2 cells in a dose-dependent manner. Autophagy inhibitor 3-methyladenine (3-MA) could reverse TGF-β1 induced autophagy process. Also, TGF-β1 significantly promotes the invasion ability of HepG2 cells; however, this process could effectively reverse by autophagy inhibitor 3-MA.
TGF-β1 enhances HepG2 cells invasion by upregulating autophagy.
研究 TGF-β1 在人肝癌 HepG2 细胞自噬和侵袭能力中的作用。
用不同浓度的 TGF-β1 处理培养的 HepG2 细胞 24 小时。用 Western blot 检测自噬相关标记物 LC3 和 Beclin1 的蛋白表达水平。用 Transwell 法检测 TGF-β1 对 HepG2 细胞侵袭能力的影响。
结果表明，TGF-β1 能够以剂量依赖的方式激活 HepG2 细胞的自噬。自噬抑制剂 3-甲基腺嘌呤（3-MA）可逆转 TGF-β1 诱导的自噬过程。此外，TGF-β1 显著促进 HepG2 细胞的侵袭能力；然而，自噬抑制剂 3-MA 可有效逆转这一过程。
TGF-β1 通过上调自噬增强 HepG2 细胞的侵袭能力。
