Wang Yun-Hsin, Chen Yau-Hung, Shen Wen-Hao
Division of Basic Research, Koo Foundation Sun Yat-Sen Cancer Center, Taipei 112, Taiwan.
Department of Chemistry, Tamkang University, Tamsui, New Taipei City 251, Taiwan.
Toxics. 2020 Nov 20;8(4):108. doi: 10.3390/toxics8040108.
(1) Background: Amikacin is an aminoglycoside antibiotic used for treating gram-negative bacterial infections in cancer patients. In this study, our aims are to investigate the migratory inhibition effects of amikacin in human MDA-MB-231 cells. (2) Methods: We used a wound-healing assay, trans-well analysis, Western blotting, immunostaining and siRNA knockdown approaches to investigate how amikacin influenced MDA-MB-231 cell migration and invasion. (3) Results: Wound healing showed that the MDA-MB-231 cell migration rates decreased to 44.4% in the presence of amikacin. Trans-well analysis showed that amikacin treatment led to invasion inhibition. Western blotting demonstrated that amikacin induced thioredoxin-interacting protein (TXNIP) up-regulation. TXNIP was knocked down using siRNA in MDA-MB-231 cell. Using immunostaining analysis, we found that inhibition of TXNIP expression led to MDA-MB-231 pseudopodia extension; however, amikacin treatment attenuated the cell extension formation. (4) Conclusions: We observed inhibition of migration and invasion in MDA-MB-231 cells treated with amikacin. This suggests inhibition might be mediated by up-regulation of TXNIP.
（1）背景：阿米卡星是一种氨基糖苷类抗生素，用于治疗癌症患者的革兰氏阴性菌感染。在本研究中，我们的目的是研究阿米卡星对人MDA-MB-231细胞的迁移抑制作用。（2）方法：我们采用划痕愈合试验、Transwell分析、蛋白质印迹法、免疫染色和小干扰RNA敲低方法，研究阿米卡星如何影响MDA-MB-231细胞的迁移和侵袭。（3）结果：划痕愈合试验显示，在存在阿米卡星的情况下，MDA-MB-231细胞迁移率降至44.4%。Transwell分析表明，阿米卡星处理导致侵袭抑制。蛋白质印迹法证明，阿米卡星诱导硫氧还蛋白相互作用蛋白（TXNIP）上调。在MDA-MB-231细胞中使用小干扰RNA敲低TXNIP。通过免疫染色分析，我们发现抑制TXNIP表达导致MDA-MB-231伪足延伸；然而，阿米卡星处理减弱了细胞延伸的形成。（4）结论：我们观察到用阿米卡星处理的MDA-MB-231细胞的迁移和侵袭受到抑制。这表明这种抑制可能是由TXNIP上调介导的。
