Genistein对人鼻咽癌细胞系CNE抑制增殖和促进凋亡的作用及机制探讨

目的:研究genistein对人鼻咽癌细胞系CNE抑制增殖和促进凋亡的作用,探讨其抗癌作用的机制。方法:应用MTT检测不同浓度genistein在不同时间对鼻咽癌细胞系CNE的生长抑制作用;透视电镜下观察鼻咽癌细胞演变过程、凋亡细胞及凋亡小体,应用流式细胞仪分析细胞周期及凋亡率。结果:Genistein可明显抑制CNE细胞的增殖,并且这种抑制作用呈时间及浓度依赖性,随浓度的增加时间的延长抑制作用逐渐增强,尤以200μmol/L组最明显;Genistein诱导鼻咽癌细胞的早期凋亡率随浓度的增加而增强,200μmol/L时为49.9%;FCM分析发现genistein阻断CNE细胞生长于细胞周期的G2/M期;电镜观察到用药后凋亡细胞典型的形态学特征。结论:Genistein对鼻咽癌细胞系CNE的生长有明显的呈时间及浓度依赖性的抑制作用,其阻断细胞的生长主要在细胞周期的G2/M期,并且具有明显诱导CNE细胞凋亡的作用。     

High mobility group box 1 (HMGB1) is upregulated by the Epstein-Barr virus infection and promotes the proliferation of human nasopharyngeal carcinoma cells

Conclusion: The current study confirmed the significant high mobility group box 1 (HMGB1) was promoted in human nasopharyngeal carcinoma (NPC) tissues by Epstein-Barr virus (EBV) infection, in association with the malignant status of NPC, and promoted the proliferation NPC cells RAGE-dependently. Objectives: The present study was to examine the association of HMGB1 over-expression in human NPC with the EBV-positivity and to determine the regulatory role of HMGB1 on the proliferation of NPC cells in vitro. Methods: Real-time PCR and Western blotting were utilized to examine the HMGB1 expression. EBV infection in CNE-2 cells was performed to investigate the HMGB1 promotion by EBV infection. RNA interference technology was utilized for the RAGE knockout. Results: It was demonstrated that HMGB1 was significantly higher in both mRNA and protein levels in the EBV-positive NPC tissues, in marked association with the malignant status of NPC, and with the LMP1 DNA level in EBV-positive NPC samples. In addition, the MTT assay, growth curve, and the colony forming assay confirmed the promotion by HMGB1 to the proliferation of CNE-2 cells, depending on RAGE.