摘要
目的:研究葛根素对人皮肤鳞状细胞癌(CSCC)中磷脂酰肌醇-3激酶(PI3K)/蛋白激酶B(AKT)信号通路激活状态的干预作用。方法:收集人CSCC组织(52例)及正常皮肤组织(35例),培养人CSCC细胞株SCL-1、A431、HSC-5和人永生化角质形成细胞株HaCaT细胞,检测p-PI3K、p-AKT的表达水平;SCL-1细胞进行分组,用不同剂量葛根素(20μmol/L、40μmol/L、80μmol/L)处理,转染阴性对照(NC)质粒或PI3K质粒,检测细胞增殖活力、侵袭数目及p-PI3K、p-AKT的表达水平;BALB/c-nu裸鼠皮下注射SCL-1细胞建立移植瘤模型,100 mg/kg葛根素灌胃处理3周后检测移植瘤质量、体积及p-PI3K、p-AKT的表达水平。结果:人CSCC组织中p-PI3K、p-AKT的表达水平高于正常皮肤组织(P<0.05);人CSCC细胞株中p-PI3K、p-AKT的表达水平高于HaCaT细胞且SCL-1中p-PI3K、p-AKT表达上调最显著(P<0.05);不同剂量葛根素处理后,SCL-1细胞的增殖活力、侵袭数目及p-PI3K、p-AKT的表达水平均降低(均P<0.05);转染质粒后,PI3K质粒+80μmol/L葛根素组SCL-1细胞的增殖活力、侵袭数目高于NC质粒+80μmol/L葛根素组(P<0.05);葛根素组裸鼠的移植瘤质量、体积及p-PI3K、p-AKT的表达水平均低于对照组(P<0.05)。结论:PI3K/AKT信号通路过度激活与CSCC发病有关,葛根素通过抑制该通路发挥抗CSCC作用。
Objective To study the intervention effect of puerarin on the activation status of phosphatidylinositol-3 kinase(PI3K)/protein kinase B(AKT) signaling pathway in human cutaneous squamous cell carcinoma(CSCC). Methods human CSCC tissues(52 cases)and normal skin tissues(35 cases) were collected, human CSCC cell lines SCL-1, A431, HSC-5 and human immortalized keratinocyte line HaCaT were cultured. Then the expression levels of p-PI3K and p-AKT were detected. SCL-1 cells were divided into groups, treated with different doses of Puerarin(20 μmol/L, 40 μmol/L, 80 μmol/L), and transfected with negative control(NC) plasmid or PI3K plasmid. Then the proliferation viability, invaded numbers, the expression levels of p-PI3K and p-AKT were detected. The transplanted tumor model was established by subcutaneous injection of SCL-1 cells into BALB/c-nu nude mice, 100 mg/kg puerarin was given by gavage for 3 weeks and the weight and volume of transplanted tumor,the expression levels of p-PI3K and p-AKT were detected. Results The expression levels of p-PI3K and p-AKT in human CSCC tissue were higher than those in normal skin tissue(P<0.05), the expression levels of p-PI3K and p-AKT in human CSCC cell line were higher than those in HaCaT cell line(P<0.05), and the expression levels of p-PI3K and p-AKT in SCL-1 were up-regulated most significantly(P<0.05). After different doses of puerarin treatment, the proliferation viability, invaded number and the expression levels of p-PI3K and p-AKT in SCL-1 cells decreased(all P<0.05).After plasmid transfection, the proliferation viability, invaded number of PI3K plasmid+80 μmol/L puerarin group were higher than those in NC plasmid+80μmol/L puerarin group(P<0.05). The weight and volume of transplanted tumor and the expression levels of p-PI3K and p-AKT in puerarin group were lower than those in control group(P<0.05). Conclusion The overactivation of PI3K/AKT signaling pathway relates to the pathogenesis of CSCC. Puerarin exerts its anti CSCC effect by inhibiting this pathway.
作者
段强
冯群燕
DUAN Qiang;FENG Qunyan(Department of Dermatology,Xianyang Central Hospital,Xianyang 712000,Shaanxi,China)
出处
《中国美容医学》
CAS
2022年第4期105-109,共5页
Chinese Journal of Aesthetic Medicine
