Enoxacin and bis-enoxacin stimulate 4T1 murine breast cancer cells to release extracellular vesicles that inhibit osteoclastogenesis.
Enoxacin and bis-enoxacin stimulate 4T1 murine breast cancer cells to release extracellular vesicles that inhibit osteoclastogenesis.
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DOI：
10.1038/s41598-018-34698-9
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发表时间：
2018-11-01
影响因子：
4.6
通讯作者：
Holliday LS
中科院分区：
文献类型：
--
作者：
Vracar TC;Zuo J;Park J;Azer D;Mikhael C;Holliday SA;Holsey D;Han G;VonMoss L;Neubert JK;Rody WJ Jr;Chan EKL;Holliday LS
依诺沙星及其趋骨双膦酸盐衍生物双依诺沙星作为治疗癌症和骨病的潜在治疗剂最近引起了人们的关注。在依诺沙星或双依诺沙星浓度为50 μM时，未检测到4 T1鼠乳腺癌细胞的生长或存活差异。在较高浓度下生长受到干扰。50 μM依诺沙星和双依诺沙星都刺激了GW/加工体数量的增加，但microRNA水平的变化很小。用50 μM依诺沙星或50 μM双依诺沙星处理的4 T1细胞释放的细胞外囊泡（EV）刺激RAW 264.7细胞的增殖，并且都显著抑制骨化三醇刺激的小鼠骨髓中的破骨细胞生成。来自用依诺沙星和双依诺沙星处理的4 T1细胞的EV显示微小RNA（miR）-146a-5p和let-7 b-5 p的量的小幅减少。与此形成鲜明对比的是，已被证明可调节骨重建的miR-214- 3 p分别增加了22倍和30倍。我们的结论是，依诺沙星和双依诺沙星触发释放的EV从4 T1癌细胞，抑制破骨细胞。
Enoxacin and its bone-seeking bisphosphonate derivative, bis-enoxacin, have recently captured attention as potential therapeutic agents for the treatment of cancer and bone disease. No differences in growth or survival of 4T1 murine breast cancer cells were detected at a concentration of 50 µM of enoxacin or bis-enoxacin. Growth was perturbed at higher concentrations. Both 50 µM enoxacin and bis-enoxacin stimulated increases in the number of GW/Processing bodies, but there were minimal changes in microRNA levels. Extracellular vesicles (EVs) released from 4T1 cells treated with 50 µM enoxacin or 50 µM bis-enoxacin stimulated proliferation of RAW 264.7 cells, and both significantly inhibited osteoclastogenesis in calcitriol-stimulated mouse marrow. EVs from 4T1 cells treated with enoxacin and bis-enoxacin displayed small reductions in the amount of microRNA (miR)-146a-5p and let-7b-5p. In marked contrast, miR-214-3p, which has been shown to regulate bone remodeling, was increased 22-fold and 30-fold respectively. We conclude that enoxacin and bis-enoxacin trigger the release of EVs from 4T1 cancer cells that inhibit osteoclastogenesis.
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