CAJ | 학술논문

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；0.5μmol/L PTX联合0.625μmol/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。
목적：연구17-AAG연합자삼순（PTX）대식관암세포Eca-109증식화조망적영향。방법여이PTX화17-AAG단독혹연합사용작용우Eca-109세포주，채용MTT법검측기세포증식적변화，응용류식세포의검측세포주기、조망적변화。결과여대조조상비，단독사용17-AAG、PTX균능구억제Eca-109세포적증식；0.5μmol/L PTX연합0.625μmol/L 17-AAG가억제Eca-109적생장，차연합효응명현강우각자단약조（P<0.01）；류식세포의검측결과현시：17-AAG장Eca-109세포조체우G2/M기，PTX장Eca-109세포조체우S기。17-AAG여PTX연합용약사Eca-109세포조체우G2/M기화S。17-AAG조、PTX조급연합조작용Eca-109세포주24 h후기조망솔분별위4.52%、10.91%、29.88%，현저고우대조조（1.32%）；연합용약후，가형성명현조망봉，명현고우단약조。결론 PTX화17-AAG균가억제식관암세포증식，유도암세포조망，량자연합가증강상술작용。
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 0.5μmol/L PTX and 0.625μmol/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.