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首页> 外文期刊>Journal of biochemical and molecular toxicology >MEG3 is restored by schisandrin A and represses tumor growth in choriocarcinoma cells
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MEG3 is restored by schisandrin A and represses tumor growth in choriocarcinoma cells

机译：由Schisandrin A恢复Meg3并抑制毒性癌细胞中的肿瘤生长

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Schisandrin A (SchA) has been reported as a multidrug resistance-reversing agent; however, its antitumor effects have been rarely reported. Consequently, we attempted to explore whether SchA per se possesses an antitumor property in choriocarcinoma JEG-3 and BeWo cells and its potential mechanisms. JEG-3, BeWo, and HTR-8/SVneo cells were stimulated with SchA at different concentrations (10-100μM), and cellular viability was evaluated with Cell Counting Kit-8. After stimulation with SchA, proliferation, apoptosis, migration, and invasion were detected by bromodeoxyuridine assay, Annexin V-fluorescein isothiocyanate/ propidium iodide (Annexin V-FITC/PI) method, and a Transwell system, in JEG-3 cells transfected with short hairpin-RNA for maternally expressed 3. Western blot was performed to quantify protein. MEG3 was examined by a quantitative reverse transcription-polymerase chain reaction. MEG3 was downregulated in choriocarcinoma tissues. SchA diminished cellular viability, decreased proliferative activity, inhibited migratory and invasive behaviors, and repressed phosphorylation of regulators of phosphatidylinositol 3 kinase/protein kinase B/nuclear factor κB (PI3K/AKT/NF-κB) signaling cascade in gestational choriocarcinoma cells. MEG3 was upregulated by SchA in JEG-3 and BeWo cells. SchA exhibited little suppressive effects in JEG-3 cells lacking MEG3. Besides, the phosphorylation of transducers was evoked in MEG3-silenced JEG-3 cells despite stimulation with SchA. SchA administration repressed the growth of JEG-3 and BeWo cells by upregulating MEG3. Besides, SchA blocked PI3K/AKT/NF-κB signal cascade by elevating MEG3.
机译：五味子素A（SCA）是一种多药耐药逆转剂；然而，其抗肿瘤作用鲜有报道。因此，我们试图探索SCA本身是否在绒毛膜癌JEG-3和BeWo细胞中具有抗肿瘤特性及其潜在机制。用不同浓度（10-100μM）的SCA刺激JEG-3、BeWo和HTR-8/SVneo细胞，并用细胞计数试剂盒-8评估细胞活力。在用SCA刺激后，通过溴脱氧尿苷试验、膜联蛋白V-荧光素异硫氰酸酯/碘化丙啶（膜联蛋白V-FITC/PI）方法和Transwell系统检测转染短发夹RNA的JEG-3细胞中的增殖、凋亡、迁移和侵袭，以获得母代表达的3。采用Western-blot法对蛋白质进行定量分析。用定量逆转录聚合酶链反应检测MEG3。MEG3在绒毛膜癌组织中表达下调。SchA降低了妊娠绒毛膜癌细胞的细胞活力，降低了增殖活性，抑制了迁移和侵袭行为，并抑制了磷脂酰肌醇3激酶/蛋白激酶B/核因子κB（PI3K/AKT/NF-κB）信号级联调节因子的磷酸化。MEG3在JEG-3和BeWo细胞中被SCA上调。SCA对缺乏MEG3的JEG-3细胞几乎没有抑制作用。此外，尽管受到SCA的刺激，MEG3沉默的JEG-3细胞中的传感器磷酸化仍被诱发。SCA通过上调MEG3抑制JEG-3和BeWo细胞的生长。此外，SchA通过升高MEG3阻断PI3K/AKT/NF-κB信号级联。

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