摘要
目的探讨生长抑素（SST）抑制人类肝癌细胞株生长的机制及对p16基因表达水平的影响。方法取液氮保存的人类肝癌细胞株HepG2培养后，随机分为三组：对照组（A组）不含SST、低浓度组（B组）SST为10^-8mol／L、高浓度组（C组）SST为10^-5mol／L，用流式细胞术（FCM）检测细胞周期，RT．PCR法检测p16基因mRNA表达变化。结果HepG2经不同浓度SST作用24h后FCM检测细胞周期发现，A组、B组、c组G。期细胞所占比例均值分别为（51．41±3．27）％、（65．43±3．41）％、（69．02±3．75）％，而s期细胞所占比例均值为（36．86±2．31）％、（20．34±2．52）％、（18．50±3．09）％，G2期细胞所占比例均值为（11．46±1．96）％、（14．23±3．83）％、（12．48±3．18）％。与A组相比，B组、c组Gt期细胞明显增多，而s期细胞相对减少。经RT—PCR法检测，各组均表达p16基因mRNA，但B组、C组表达明显增强。结论SST对人类肝癌细胞的抑制可能是通过提高p16基因表达而发挥作用的。
Objective To study the effect of somatostatin on the Proliferation in Human HepG2 Cells and the Level of Gene p16. Methods The cell line HepG2 were divided into 3 groups： control groupA, low concentration group B and high concentration group C. The flow cytometry （FCM） was used to detect phase distribution of the cycles and detect the expression of p16 gene by using RT-PCR. Results Human HepG2 cells affected 24 hours later by different density SST, using FCM, we discovered that the G1 cell cycles of each A group, B group, C group occupied the proportion respectively is （51.41±3.27）%, （65.43±3.41）%, （69.02± 3.75）%, that the S cell cycles is （36.86±2.31）%, （20.34±2.52）%, （18.50±3.09）%, that the G2 cell cycles is （11.46±1.96）%, （14.23±3.83）%, （12.48±3.18）%. Compare to the control groupA, the G1 cell cycles of groupB and group C were increased obviously. But the S cell cycles relatively reduced. The levels of p16 gene were expressed in each group detected by RT-PCR, but B group and C group expressed obviously. Conclusion The inhibited mechanism of somatostatin for HepG2 was expressed probably by improving levels of p16.
出处
《肿瘤研究与临床》
CAS
2010年第11期758-760,共3页
Cancer Research and Clinic
