data in brief_γ-Tocotrienol Inhibits Cervical Cancer HeLa Cells Growth through Regulating the PI3K/AKT/mTOR Signaling Pathway

The file is a Data in Brief used by Xu et al study forγ-Tocotrienol Inhibits Cervical Cancer HeLa Cells Growth through Regulating the PI3K/AKT/mTOR Signaling Pathway in vitro. The data showed that γ-T3 (30-60 μM, especially at 45 μM) treatment significantly inhibited HeLa cellular proliferation, and its IC50 was 37.40 ± 5.70 µM at 48 hours. It induced apoptosis and increased the proportion of cells in G0/G1 phase and decreased the proportion at S phase in HeLa cells. The treatment decreased the levels of both phosphorylated and non-phosphorylated (+/-p) mTOR, upstream regulatory factors of PI3K, (+/-p) AKT, downstream regulatory factors of (+/-p) p70S6K, (+/-p) 4E-BP1 and targeted genes of Cyclin D1 and c-Myc related to HeLa cell proliferation and apoptosis. These effects of γ-T3 on the HeLa cells were similar to the actions of Wortmannin (WM), a known blocker of the PI3K/AKT/mTOR signaling pathway. Furthermore, the combination of γ-T3 and WM displayed a strong synergistic effect. These results suggest that γ-T3 could inhibit cell growth by down-regulating the PI3K/AKT/mTOR signaling pathway in human cervical cancer HeLa cells.

该文件为《数据简报》，由Xu等人在研究“γ-生育酚抑制人宫颈癌细胞HeLa生长通过调控体外PI3K/AKT/mTOR信号通路”中使用。研究数据表明，γ-T3（30-60 μM，尤其是45 μM浓度）处理显著抑制了HeLa细胞的增殖，其在48小时时的半抑制浓度（IC50）为37.40 ± 5.70 µM。该处理诱导了细胞凋亡，增加了HeLa细胞处于G0/G1期的细胞比例，并减少了S期细胞比例。治疗降低了mTOR及其上游调控因子PI3K、AKT及其下游调控因子（±p）p70S6K、（±p）4E-BP1以及与HeLa细胞增殖和凋亡相关的Cyclin D1和c-Myc靶基因的水平。γ-T3对HeLa细胞的作用与已知PI3K/AKT/mTOR信号通路阻断剂Wortmannin（WM）的作用相似。此外，γ-T3与WM的联合应用表现出显著的协同效应。这些结果表明，γ-T3可能通过下调人宫颈癌细胞HeLa中的PI3K/AKT/mTOR信号通路来抑制细胞生长。