17-AAG联合紫杉醇对Eca-109食管癌细胞增殖的抑制作用

目的研究17-AAG联合紫杉醇（PTX）对食管癌细胞Eca-109增殖和凋亡的影响。方法予以PTX和17-AAG单独或联合
使用作用于Eca-109细胞株，采用MTT法检测其细胞增殖的变化，应用流式细胞仪检测细胞周期、凋亡的变化。结果与对照组
相比，单独使用17-AAG、PTX均能够抑制Eca-109细胞的增殖；0.5 μmol/L PTX联合0.625 μmol/L 17-AAG可抑制Eca-109的生
长，且联合效应明显强于各自单药组（P<0.01）；流式细胞仪检测结果显示：17-AAG将Eca-109 细胞阻滞于G2/M 期，PTX将
Eca-109 细胞阻滞于S 期。17-AAG与PTX 联合用药使Eca-109 细胞阻滞于G2/M 期和S。17-AAG组、PTX组及联合组作用
Eca-109细胞株24 h后其凋亡率分别为4.52%、10.91%、29.88%，显著高于对照组（1.32%）；联合用药后，可形成明显凋亡峰，明显高
于单药组。结论PTX和17-AAG均可抑制食管癌细胞增殖，诱导癌细胞凋亡，两者联合可增强上述作用。

Inhibitory effect of 17-AAG combined with paclitaxel on proliferation of esophageal squa-mous cell carcinoma Eca-109 cells in vitro

Objective To investigate the effect of 17-AAG combined with paclitaxel (PTX) on the proliferation and apoptosis of
esophageal squamous cell carcinoma cell line Eca-109 in vitro. Methods Eca-109 cells were treated with 17-AAG and PTX either
alone or in combination. The proliferation of Eca-109 cells was detected by MTT assay, and the cell cycle changes and cell
apoptosis were determined by flow cytometry. Results Compared with the control group, both 17-AAG and PTX significantly
inhibited the proliferation of Eca-109 cells. A combined treatment of the cells with 0.5 μmol/L PTX and 0.625 μmol/L 17-AAG
produced an obviously stronger inhibitory effect on the cell proliferation than either of the agents used alone (P<0.01). Flow
cytometry showed that, 17-AAG and PTX used alone caused Eca-109 cell cycle arrest in G2/M phase and S phase, respectively,
and their combined use caused cell cycle arrest in both G2/M and S phases. The cell apoptosis rates of Eca-109 cells treated with
17-AAG, PTX and their combination were 4.52%, 10.91%, and 29.88%, respectively, all significantly higher than that in the
control group (1.32%); the combined treatment resulted in a distinct apoptotic peak that was significantly higher than that
caused by either of the agents alone. Conclusion 17-AAG and PTX can inhibit cell proliferation and promote apoptosis of
Eca-109 cells, and their combination produces stronger effects in inhibiting cell proliferation and increasing cell apoptosis.