摘要
目的 研究香菇多糖(LNT)通过调控磷脂酰肌醇-3激酶/蛋白激酶B(PI3K/Akt)信号通路对甲状腺癌细胞生物学行为的影响。方法 将甲状腺癌TPC-1细胞分为空白组(常规培养)和低、中、高剂量实验组(20、40、60μmol·L^(-1)LNT);另用不同剂量PI3K抑制剂LY294002(0、5 mg·L^(-1))处理甲状腺癌TPC-1细胞,根据浓度分为对照组和LY294002组。以噻唑蓝(MTT)法检测细胞增殖能力,以Transwell实验检测细胞迁移及侵袭情况,以流式细胞术检测细胞凋亡及细胞周期,以蛋白质印迹法检测PI3K、磷酸化PI3K(p-PI3K)、Akt、磷酸化Akt(p-Akt)蛋白表达。结果 香菇多糖可呈时间及浓度依赖性抑制甲状腺癌TPC-1细胞增殖率(P<0.05)。空白组和低、中、高剂量实验组细胞迁移数分别为(127.67±8.09)、(98.00±5.76)、(77.67±6.25)、(38.33±5.13)个;细胞侵袭数分别为(144.50±12.50)、(109.67±6.02)、(83.00±8.07)、(50.00±4.65)个;细胞凋亡率分别为(5.82±1.37)%、(15.03±1.97)%、(26.86±2.57)%、(37.97±3.32)%;S期百分比分别为(32.09±2.49)%、(26.68±1.55)%、(21.07±2.19)%、(14.36±1.15)%,G2/M期百分比分别为(18.74±3.55)%、(16.47±3.62)%、(12.96±4.39)%、(12.41±1.66)%,G0/G1期百分比分别为(49.17±1.58)%、(56.86±2.37)%、(65.97±2.81)%、(73.23±1.63)%;低、中、高剂量实验组与空白组相比,差异均有统计学意义(均P<0.05)。与对照组相比,LY294002组能抑制TPC-1细胞增殖、迁移和侵袭,促进TPC-1细胞凋亡(均P<0.05);与对照组相比,LY294002组G0/G1期细胞百分比升高,S期、G2/M期细胞百分比降低(均P<0.05)。结论 LNT可能通过PI3K/Akt信号通路抑制甲状腺癌细胞的增殖、迁移及侵袭,诱导其凋亡,阻滞细胞周期。
Objective To investigate the effect of lentinan(LNT)on the biological behavior of thyroid cancer cells by regulating phosphatidylinositol 3-hydroxykinase/protein kinase B(PI3K/Akt)signaling pathway.Methods Thyroid carcinoma TPC-1 cells were divided into blank group(normal culture)and low,medium,high dose experimental groups(20,40,60μmol·L^(-1) LNT).In addition,thyroid cancer TPC-1 cells were treated with different doses of PI3K inhibitor LY294002(0,5 mg·L^(-1)),and divided into control group and LY294002 group according to the concentration.Cell migration and invasion were detected by methyl thiazolyl tetrazolium(MTT),cell migration and invasion were detected by Transwell,cell apoptosis and cell cycle were detected by flow cytometry,and the protein expressions of PI3K,phosphorylated PI3K(p-PI3K),Akt and phosphorylated Akt(p-Akt)were detected by Western blot.Results LNT could inhibit the proliferation rate of thyroid carcinoma TPC-1 cells in a time and concentration dependent manner(P<0.05).The number of cell migration in blank group and low,medium,high dose experimental groups were 127.67±8.09,98.00±5.76,77.67±6.25 and 38.33±5.13;the number of cells invaded were 144.50±12.50,109.67±6.02,83.00±8.07 and 50.00±4.65;the apoptosis rates were(5.82±1.37)%,(15.03±1.97)%,(26.86±2.57)%and(37.97±3.32)%;percentage of cells in S phase were(32.09±2.49)%,(26.68±1.55)%,(21.07±2.19)%and(14.36±1.15)%;percentage of cells in G2/M phase were(18.74±3.55)%,(16.47±3.62)%,(12.96±4.39)%and(12.41±1.66)%;percentage of cells in G0/G1 phase were(49.17±1.58)%,(56.86±2.37)%,(65.97±2.81)%,(73.23±1.63)%,low,medium and high dose experimental groups compared with blank group,the difference were statistical difference(P<0.05).Compared with control group,the PI3K/Akt pathway inhibitor LY294002 inhibited the proliferation,migration and invasion of TPC-1 cells and promoted the apoptosis of TPC-1 cells(P<0.05).Compared with the control group,the percentage of cells in GO/G1 phase was increased,and the percentage of cells in S
作者
黄文泉
何礼荣
邵益森
HUANG Wen-quan;HE Li-rong;SHAO Yi-sen(Department of Oral Trauma and Plastic Surgery,Affiliated Hospital of Jiangxi Universityof Traditional Chinese Medicine,Nanchang 330006,Jiangxi Province,China)
出处
《中国临床药理学杂志》
CAS
CSCD
北大核心
2023年第17期2502-2506,共5页
The Chinese Journal of Clinical Pharmacology
基金
江西省中医药管理局科技计划基金资助项目(2022B155)。
关键词
甲状腺癌
香菇多糖
磷脂酰肌醇3-激酶/蛋白激酶B信号通路
细胞增殖
thyroid carcinoma
lentinan
phosphatidylinositol 3-hydroxykinase/protein kinase B signaling pathway
cell proliferation
