The Research Core, Second Hospital, The Second Clinical School, Nanjing Medical University, Nanjing, Jiangsu, China.
Mol Cell Biochem. 2012 Oct;369(1-2):157-65. doi: 10.1007/s11010-012-1378-8. Epub 2012 Jul 4.
Epidermal growth factor (EGF) in high concentrations induces apoptosis of the tumor cells which express high levels of epidermal growth factor receptor. However, the precise mechanism for this induction is not clear. Galectin-3 is the most probable candidate for mediating this effect, as it is known to induce anti-apoptotic activity in a variety of tumor cells exposed to diverse apoptotic stimuli. In this study, we determined whether galectin-3 plays a role in high concentrations of EGF-induced apoptosis of HepG2 cells. We found that EGF in high concentrations led to the growth inhibition of HepG2 cells, which were associated with promotion of cell death. High concentrations of EGF suppressed cytoplasmic expression of galectin-3. Moreover, we demonstrated overexpression of galectin-3 could reduce EGF-induced apoptosis in HepG2 cells. Our study demonstrated for the first time that downregulation of cytoplasmic galectin-3 was essential for high concentrations of EGF-induced apoptosis in HepG2 cells.
表皮生长因子（EGF）在高浓度时诱导表达高水平表皮生长因子受体的肿瘤细胞凋亡。然而，这种诱导的确切机制尚不清楚。半乳糖凝集素-3是介导这种效应的最可能的候选者，因为已知它在各种暴露于不同凋亡刺激的肿瘤细胞中诱导抗凋亡活性。在这项研究中，我们确定半乳糖凝集素-3是否在高浓度 EGF 诱导的 HepG2 细胞凋亡中发挥作用。我们发现高浓度的 EGF 导致 HepG2 细胞的生长抑制，这与促进细胞死亡有关。高浓度的 EGF 抑制了半乳糖凝集素-3 的细胞质表达。此外，我们证明了过表达半乳糖凝集素-3可以减少 EGF 诱导的 HepG2 细胞凋亡。我们的研究首次表明，细胞质半乳糖凝集素-3 的下调对于高浓度 EGF 诱导的 HepG2 细胞凋亡是必不可少的。
