CAJ | 학술논문

目的：本文主要研究过表达S期激酶相关蛋白2（Skp2）能否影响曲格列酮（TRG）对乳腺癌细胞的敏感性，致力于发展一种新的药物来提高患者的生存率，最终达到治愈的目的。方法荧光报告基因方法观察过氧化物酶体增殖物激活受体（PPAR）γ型转录活性的变化；流式细胞和CCK‐8法研究Skp2过表达影响 TRG对乳腺癌细胞生长和凋亡的改变。结果 Skp2过表达能抑制PPARγ的活性，耐受TRG对乳腺癌细胞生长和凋亡的影响。结论 Skp2过表达的乳腺癌细胞能耐受TRG的敏感性，因此通过下调Skp2可能会增强TRG对乳腺癌细胞的生长抑制。
목적：본문주요연구과표체S기격매상관단백2（Skp2）능부영향곡격렬동（TRG）대유선암세포적민감성，치력우발전일충신적약물래제고환자적생존솔，최종체도치유적목적。방법형광보고기인방법관찰과양화물매체증식물격활수체（PPAR）γ형전록활성적변화；류식세포화CCK‐8법연구Skp2과표체영향 TRG대유선암세포생장화조망적개변。결과 Skp2과표체능억제PPARγ적활성，내수TRG대유선암세포생장화조망적영향。결론 Skp2과표체적유선암세포능내수TRG적민감성，인차통과하조Skp2가능회증강TRG대유선암세포적생장억제。
Objective To investigate the effects of Skp2 overexpression on the sensitivity of troglitazone (TRG) in breast cancer cells and to devote to develop a novel drug for increasing the patient survival rate and eventually reaching the cure goal .Methods The transcription activities of PPARγ were analyzed on peroxisome proliferators response element(PPRE) luciferase reporter .The flow cytometry analysis and CCK‐8 assay were adopted to study that overexpression of Skp2 was associated with resistance to TRG‐mediated inhibition growth and apoptosis of breast cancer cells .Results Our study found that overexpression of Skp2 inhibi‐ted the transcriptional activity of the endogenous PPARγ and resisted to TRG‐mediated inhibition growth and apoptosis of breast cancer cells .Conclusion Overexpressed Skp2 breast cancer cells is able to be resistant to TRG‐induced sensitivity of breast cancer cells .Furthermore down‐regulating Skp2 will significantly enhance the growth inhibition of TRG on breast cancer cells .