摘要
目的探讨过氧化物酶体增殖物激活受体-γ(PPAR-γ)对口腔癌SCC15细胞侵袭转移能力的影响及机制。方法口腔癌SCC15细胞经PPAR-γ激动剂罗格列酮处理后,以细胞黏附试验检测肿瘤细胞体外黏附能力的变化,Transwell试验检测肿瘤细胞体外侵袭能力的变化,流式细胞仪检测肿瘤细胞细胞周期的变化,Western blot试验检测肿瘤细胞E-cadherin、MMP-2/9、cyclin B以及NF-κB蛋白表达的变化,real-time PCR试验检测肿瘤细胞E-cadherin、MMP-2/9、cyclin B以及NF-κB mRNA表达的变化,报告基因技术检测NF-κB启动子活性的变化。结果肿瘤细胞经过10μg/ml及20μg/ml罗格列酮处理后,黏附能力分别下降到58.3%和37.7%;侵袭能力分别下降到35.3%和18.5%;细胞周期阻滞在G2/M期,G2/M期细胞上升到194.4%和238.9%;E-cadherin蛋白表达显著上调,MMP-2/9、cyclin B以及NF-κB蛋白表达显著下降;E-cadherin mR-NA表达分别上调到234.9%和477.6%,MMP-2 mRNA表达分别下降到74.7%和32.0%,MMP-9 mRNA表达分别下降到82.7%和23.2%,cyclin B mRNA表达分别下降到32.8%和17.9%,NF-κB mRNA表达分别下降到49.2%和26.8%;NF-κB启动子活性分别下降到63.5%和31.4%。结论 PPAR-γ可抑制人口腔癌SCC15细胞体外侵袭能力,其机制可能与其下调细胞NF-κB表达和活性,降低MMP-2/9和cyclin B表达,提高E-cadherin表达有关。
Objective To explore the effect of peroxisome proliferators activated receptors γ （PPAR-γ） on the metastasis of SCC15 cells and its mechanism. Methods After the human mouth cancer SCC15 cells were treated by PPAR-γ agonist rosiglitazone,the ad-hesion in vitro was detected by cell adhesion assay, the invasion in vitro was detected by Transwell assay,the cell cycle was detected by flow cytometry,the expression of E-cadherin, MMP-2/9, cyclin B and NF-KB was detected by Western blot and RT-PCR, and the activi-ty of NF-κB promoter was detected by reporter genes assay. Results After treated by 10 μg/ml and 20μg/ml rosiglitazone,the adhe-sion of cells in vitro was decreased to 58.3% and 37.7% ,respectively;the invasion in vitro was decreased to 35.3% and 18.5% ;cells in G2/M phase were increased to 194.4% and 238.9% ;the protein expression of E-cadherin was increased and the protein expression of MMP-2/9, cyclin B and NF-KB was decreased; the mRNA expression of E-cadherin was increased to 234.9% and 477.6%; the mRNA expression of MMP-2 was decreased to 74.7% and 32.0%, the mRNA expression of MMP-9 was decreased to 82.7% and 23.2% ,the mRNA expression of cyclin B was decreased to 32.8% and 17.9%, the mRNA expression of NF-κB was decreased to 49.2% and 26.8% ,and the activity of NF-KB promoter was decreased to 63.5% and 31.4%, respectively. Conclusion PPAR-γ, could inhibit the metastasis of SCC15 by inhibiting the expression and activity of NF-κB, down-regulating the expression of MMP-2/9, cyclin B and NF-KB, and up-regulating the expression of E-cadherin.
出处
《山西医科大学学报》
CAS
2012年第11期817-821,共5页
Journal of Shanxi Medical University
