PDCD4对甲状腺癌SW579细胞调亡及成瘤能力的影响

目的 研究程序性细胞死亡因子4(PDCD4)诱导的对甲状腺癌SW579细胞凋亡效应及抑制成瘤能力的可能作用机制.方法 将对数生长期的细胞分为两组,观察组先予以PDCD4凋亡相关基因Bax的刺激14 h进行细胞的收集,然后加入tPA刺激细胞进行收集.对照组未加PDCD4凋亡相关基因Bax的刺激和tPA刺激.应用AnnexinV/PI和API等标记,Cyclins/DNA双标流式细胞仪检测甲状腺癌SW579细胞的凋亡及周期特异性,运用RT-PCR的方法检查Caspase-3、Caspase-9活化情况.结果 处于静止期的外周血对PDCD4凋亡诱导不敏感,而G1期PDCD4诱导甲状腺癌SW579细胞出现了明显的细胞凋亡.PDCD4诱导的细胞凋亡主要是在细胞周期的G1期发生.观察组的Caspase-3、Caspase-9 mRNA的表达值分别为(1.12±0.56)、(1.10±0.29),显著高于对照组的(0.82±0.31)、(0.72±0.26),差异有统计学意义(P<0.05).结论 PDCD4诱导的细胞凋亡与甲状腺癌SW579细胞的细胞周期相关,存在G1期细胞周期阻滞的周期特异性,且此过程中发生了Caspase活化,参与细胞凋亡及可能抑制细胞成瘤能力.

Effect of PDCD4 on apoptosis and tumorigenic capacity of SW579 thyroid cancer cells

Objective To study the mechanism of programmed cell death 4 (PDCD4)-induced apoptosis and in-hibition of tumorigenic capacity in SW579 thyroid cancer (TC) cells. Methods SW579 thyroid cancer cells in logarith-mic growth phase were divided into two groups. Cells in the observation group were stimulated by PDCD4 apoptosis-relat-ed gene Bax for 14 hours and then by tPA for collection. Cells in the control group did not received stimulation by Bax and tPA. AnnexinV/PI, API markers and Cyclins/DNA flow cytometry were used to check apoptosis and cycle specificity of SW579 cells. RT-PCR was applied to check the activation conditions of Caspase-3, Caspase-9. Results SW579 cells of peripheral blood in stationary phase were not sensitive to PDCD4 induction, while those in G1 phase showed significant apoptosis under PDCD4 induction. PDCD4-induced apoptosis mainly occurred in the G1 phase. The expression levels of Caspase-3, Caspase-9 mRNA in the observation group were (1.12 ± 0.56), (1.10 ± 0.29), which were significantly higher than those in the control group of (0.82±0.31), (0.72±0.26), P<0.05. Conclusion PDCD4-induced apoptosis of SW579 cells is related to cell cycle, with cycle specificity of cell cycle arrest in G1 phase. During the cell cycle arrest, Caspase ac-tivation occurred and is involved in the apoptosis and inhibition of tumorigenic capacity.