Methyl 2-trifluoromethyl-3,11-dioxo-18β-olean-1,12-dien-3-oate (CF3DODA-Me) is derived synthetically from glycyrrhetinic acid, a major component of licorice, and this compound induced reactive oxygen species (ROS) in RD and Rh30 rhabdomyosarcoma (RMS) cells. CF3DODA-Me also inhibited growth and invasion and induced apoptosis in RMS cells, and these responses were attenuated after cotreatment with the antioxidant glutathione, demonstrating the effective anticancer activity of ROS in RMS. CF3DODA-Me also downregulated expression of specificity protein (Sp) transcription factors Sp1, Sp3, and Sp4 and prooncogenic Sp-regulated genes including PAX3-FOXO1 (in Rh30 cells). The mechanism of CF3DODA-Me-induced Sp-downregulation involved ROS-dependent repression of c-Myc and cMyc-regulated miR-27a and miR-17/20a, and this resulted in induction of the miRNA-regulated Sp repressors ZBTB4, ZBTB10, and ZBTB34. The cell and tumor growth effects of CF3DODA-Me further emphasize the sensitivity of RMS cells to ROS inducers and their potential clinical applications for treating this deadly disease. IMPLICATIONS: CF3DODA-Me and HDAC inhibitors that induce ROS-dependent Sp downregulation could be developed for clinical applications in treating rhabdomyosarcoma.

译文

:2-三氟甲基-3,11-二氧杂-18β-油酸酯-1,12-二烯-3-酸酯(CF3DODA-Me)合成自甘草酸的主要成分甘草次酸,该化合物可诱导活性氧(ROS)在RD和Rh30横纹肌肉瘤(RMS)细胞中。 CF3DODA-Me还抑制RMS细胞的生长和侵袭并诱导细胞凋亡,在与抗氧化剂谷胱甘肽共同处理后,这些反应减弱,证明ROS在RMS中具有有效的抗癌活性。 CF3DODA-Me还下调了特异性蛋白(Sp)转录因子Sp1,Sp3和Sp4的表达以及包括PAX3-FOXO1在内的促癌性Sp调控的基因(在Rh30细胞中)。 CF3DODA-Me诱导的Sp下调的机制涉及ROS依赖的c-Myc和cMyc调节的miR-27a和miR-17 / 20a的阻遏作用,这导致了miRNA调节的Sp阻遏物ZBTB4,ZBTB10,和ZBTB34。 CF3DODA-Me对细胞和肿瘤的生长作用进一步强调了RMS细胞对ROS诱导剂的敏感性及其在治疗这种致命疾病中的潜在临床应用。结论:可以诱导ROS依赖性Sp下调的CF3DODA-Me和HDAC抑制剂可用于治疗横纹肌肉瘤的临床应用。

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