| 李静,刘芳.甲氟奎对食管鳞癌细胞增殖、迁移和侵袭的影响及其机制[J].安徽医药,2021,25(6):1065-1069. |
| 甲氟奎对食管鳞癌细胞增殖、迁移和侵袭的影响及其机制 |
| Mechanism of mefloquine regulating proliferation, migration and invasion of esophageal squamous carcinoma cells |
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| DOI：10.3969/j.issn.1009-6469.2021.06.002 |
| 中文关键词: 食管肿瘤 甲氟奎 β-catenin信号通路 增殖 迁移 侵袭 |
| 英文关键词: Esophageal neoplasms Mefloquine β-catenin signaling pathway Proliferation Migration Invasion |
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| 中文摘要: |
| 目的研究甲氟奎对食管鳞癌细胞增殖、迁移和侵袭的影响及其机制。方法运用四甲基偶氮唑盐微量酶反应比色法( MTT法)法检测甲氟奎( 5、10、15、30 μmol/L)对食管鳞癌细胞 KYSE140的增殖的调控，筛选最适浓度 30 μmol/L；用 β连环素( β-catenin)信号通路激活剂 Wnt3a或二甲基亚砜( DMSO)与 30 μmol/L甲氟奎共处理 KYSE140细胞 48 h。Transwell法检测细胞的迁移和侵袭；蛋白质印迹法( Western blotting)检测细胞中 β-catenin、周期素依赖激酶抑制剂 p21、增殖细胞核抗原( PCNA)、神经钙黏素( N-cadherin)、上皮钙黏素( E-cadherin)的蛋白表达；实时荧光定量逆转录聚合酶链反应( qRT-PCR)检测细胞中 β-catenin的表达。结果甲氟奎可呈浓度依赖性抑制食管鳞癌细胞 KYSE140的增殖，最适浓度为 15 μmol/L；在 24、48和 72 h时对照组细胞吸光度分别为( 0.21±0.02)、(0.52±0.04)、(1.19±0.10)15 μmol/L甲氟奎组细胞吸光度分别为( 0.21±0.01)、(0.34±0.03)、(0.68±0.06)；对照组迁移和侵袭细胞数分别为( 120±8)个0±6)个，甲氟奎组迁移和侵袭细胞数分别为( 62±5)个、(45±4)个，甲氟奎可明显的抑制 KYSE140细胞的增殖、迁移和侵袭，上调 p21、E-cadherin，下调 PCNA、N-cadherin；最重要的是，甲氟奎可明显的抑制 β-catenin信号通路的关键基因 β-catenin的表达，且激活 β-catenin信号通路可逆转甲氟奎对 KYSE140细胞的增殖、迁移和侵袭的抑制。结论甲氟奎可抑制食管鳞癌细胞的增殖、迁移和侵袭，其机制与抑制 β-catenin信号通路、(8，的活性相关，将可为甲氟奎治疗食管鳞癌提供更充分的依据。 |
| 英文摘要: |
| Objective To study the effect and mechanism of mefloquine on proliferation, migration and invasion of esophageal squamous carcinoma cells.Methods The methyl thiazolyl tetrazolium (MTT) method was used to detect the regulation of mefloquine (5, 10,15, 30 μmol/L) on the proliferation of esophageal squamous cell carcinoma KYSE140, and the optimal concentration was 30 μmol/L. βcatenin signaling pathway activator Wnt3a or dimethyl sulfoxide (DMSO) and 30 μmol/L mefloquine co-treated KYSE140 cells for 48h. Transwell method was used to detect cell migration and invasion; Western blotting was used to detect the expression levels of βcatenin, cyclin-dependent kinase inhibitor p21, proliferating cell nuclear antigen (PCNA), neural cadherin (N-cadherin), and epithelial cadherin (E -cadherin).Real-time fluorescent quantitative polymerase chain reaction (qRT-PCR) was adopted to detect the expression of β-catenin in cells.Results Mefloquine inhibited the proliferation of esophageal squamous cell carcinoma KYSE140 in a concentration-dependent manner. The optimal concentration was 15 μmol/L.The A450 nm values of cells in the control group at 24, 48 and 72 h were (0.21±0.02), (0.52±0.04), (1.19±0.10), and the A450 nm values of cells in the 15 μmol/L mefloquine group were: (0.21 ±0.01),(0.34±0.03), (0.68±0.06).The number of migrant and invasive cells in the control group were (120±8) and (80±6), respectively, whilethe number of migrant and invasivecells in the mefloquine group were (62±5) and (45±4). Mefloquine significantly inhibited the proliferation, migration and invasion of KYSE140 cells, up-regulated p21 and E-cadherin,and down-regulated PCNA and N-cadherin.What was most important is thatmefloquine could significantly inhibit the expression of β-catenin, a key gene in the β-catenin signaling pathway, and activation of the β-catenin signaling pathway could reverse the inhibition of proliferation, migration and invasion of KYSE140 cells by mefloquine.Conclusion Mefloquine can inhibit the proliferation, migration and invasion of esophageal squamous carcinomacells, and its mechanism is related to the inhibition of β-catenin signaling pathway, which will provide a more sufficient basis for the treatment of esophageal squamous carcinoma. |
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