| 王书芬,倪猛,薛萌.生长抑素联合人转录因子叉头框蛋白 D1通过磷脂酰肌醇 3激酶 /蛋白激酶 B通路调控胰腺癌细胞增殖、迁移和侵袭的机制研究[J].安徽医药,2022,26(10):1919-1924. |
| 生长抑素联合人转录因子叉头框蛋白 D1通过磷脂酰肌醇 3激酶 /蛋白激酶 B通路调控胰腺癌细胞增殖、迁移和侵袭的机制研究 |
| Study on the mechanism of somatostatin combined with human transcription factor forkhead box protein D1 in regulating the proliferation, migration and invasion of pancreatic cancer cells through the phosphatidylinositol 3-kinase/protein kinase B pathway |
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| DOI：10.3969/j.issn.1009-6469.2022.10.003 |
| 中文关键词: 生长抑素 胰腺肿瘤 人转录因子叉头框蛋白 D1(FOXD1) 磷脂酰肌醇 3激酶 /蛋白激酶 B通路( PI3K/AKT通路) |
| 英文关键词: Somatostatin Pancreatic neoplasms FOXD1 PI3K/AKT pathway |
| 基金项目:南阳市科技攻关项目( 192102310326) |
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| 中文摘要: |
| 目的探讨生长抑素联合人转录因子叉头框蛋白 D1(FOXD1)通过磷脂酰肌醇 3激酶 /蛋白激酶 B(PI3K/AKT)通路调控胰腺癌细胞增殖、迁移和侵袭的机制研究。方法研究于 2018年 12月至 2019年 12月进行，通过体外培养 PANC-1细胞，过不同浓度( 0 mg/L、100 mg/L、200 mg/L、400 mg/L)的生长抑素( SST)处理细胞，记为生长抑素各剂量组，其中 0 mg/L和 400 mg/经L的生长抑素作为对照组( Control)和生长抑素组( SST)；将过表达载体( pcDNA)和过表达 FOXD1(FOXD1)转染至 PANC-1细胞，经过 400 mg/L的生长抑素及 20 mol/L的 PI3K抑制剂 LY294002处理细胞，记为 SST+pcDNA组、 SST+FOXD1组和 SST+ FOXD1+LY294002组。四甲基偶氮唑盐微量酶反应比色法( MTT)检测细胞增殖； Transwell检测细胞迁移和侵袭；蛋白质印迹法( Western blotting)检测增殖细胞核抗原( PCNA)、基质金属蛋白酶 -2(MMP-2)、基质金属蛋白酶 -9(MMP-9)、 FOXD1和 PI3K/ AKT相关蛋白的表达；实时荧光定量逆转录聚合酶链反应( qRT-PCR)检测 FOXD1 mRNA的表达。结果与 Control组相比， SST组可以抑制 FOXD1 mRNA(0.47±0.03)及蛋白表达( 0.42±0.04)、增殖( 0.52±0.05)、迁移( 66.8±7.2)和侵袭( 63.7±6.5)能力，下调 p-PI3K(0.43±0.04)、 p-AKT(0.39±0.03)蛋白表达；与 SST+pcDNA组相比， SST+FOXD1组可以促进以抑制 FOXD1 mRNA(0.67±0.05)及蛋白表达( 0.64±0.06)、增殖( 0.71±0.07)、迁移( 86.9±8.5)和侵袭( 81.5±7.3)能力，上调 p-PI3K(0.62±0.05)、 p-AKT(0.65±0.06)蛋白表达。与 SST+FOXD1组相比， SST+FOXD1+LY294002组可以抑制 FOXD1 mRNA(0.37±0.04)及蛋白表达(0.35±0.03)、增殖( 0.53±0.05)迁移(67.2±6.5)和侵袭( 62.5±5.2)。结论生长抑素通过调控 FOXD1的表达抑制胰腺癌细胞增殖、迁移和侵袭，其作用机制可能与抑制 PI3K/AKT通路有关。 |
| 英文摘要: |
| Objective To investigate the mechanism of somatostatin combined with human transcription factor forkhead box protein D1 (FOXD1) regulating the proliferation, migration and invasion of pancreatic cancer cells through the phosphatidylinositol 3-kinase/ protein kinase B (PI3K/AKT) pathway.Methods The experiment was conducted from December 2018 to December 2019, PANC-1 cells were cultured in vitro, and treated with somatostatin (SST) at different concentrations (0 mg/L, 100 mg/L, 200 mg/L, 400 mg/L), andthe cells were recorded as somatostatin dose groups, among them, 0 mg/L and 400 mg/L somatostatin were used as the control group(Control) and somatostatin group (SST); the transfection of overexpression vector (pcDNA) and overexpression FOXD1 (FOXD1) intoPANC-1 cells, and the cells were treated with 400 mg/L somatostatin and 20 mol/L PI3K inhibitor LY294002, denoted as SST+pcDNAgroup, SST+FOXD1 group, and SST+FOXD1+LY294002 group. Colorimetric method of microenzyme reaction of tetramethylazazole salt(MTT) detected cell proliferation; Transwell detected cell migration and invasion; Western blot detected the expression of proliferatingcell nuclear antigen (PCNA), matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase (MMP-9), FOXD1 and PI3K/AKT related protein; real-time fluorescence quantitative reverse transcription polymerase chain reaction (qRT-PCR) detected the expression of FOXD1 mRNA.Results Compared with the Control group, the SST group could inhibit FOXD1 mRNA (0.47±0.03) and protein (0.42±0.04)expression, proliferation (0.52±0.05), migration (66.8±7.2) and invasion (63.7±6.5), and down-regulate the expression of p-PI3K (0.43±0.04) and p-AKT (0.39±0.03) protein; compared with the SST+pcDNA group, the SST+FOXD1 group could promote and suppressFOXD1 mRNA (0.67±0.05) and protein (0.64±0.06) expression, proliferation (0.71±0.07), migration (86.9±8.5) and invasion (81.5±7.3),up-regulation of p-PI3K (0.62±0.05), p-AKT (0.65±0.06) protein expression. Compared with the SST+FOXD1 group, the SST+FOXD1+LY294002 group could inhibit FOXD1 mRNA (0.37±0.04) and protein (0.35±0.03) expression, proliferation (0.53±0.05), migration(67.2±6.5) and invasion (62.5±5.2).Conclusion Somatostatin inhibits the proliferation, migration and invasion of pancreatic cancercells by regulating the expression of FOXD1, and its mechanism may be related to the inhibition of the PI3K/AKT pathway. |
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