Tricin, a natural flavonoid present in large amounts in rice bran, was investigated for the mechanisms by which it exhibited antiproliferation and anti-invasion in C6 glioma cells. The results indicated that treatment with 5, 10, 25, and 50 μM tricin for 48 h significantly (p < 0.05) inhibited cell numbers and colony numbers with values of 134.3 ± 5.5, 114.6 ± 2.5, 106.3 ± 3.2, and 57.3 ± 10.2, respectively. Tricin also inhibited C6-cell motility, migration, and invasion. Tricin changed the cytoskeletal organization, reduced matrix-metalloproteinase (MMP) expression, and upregulated E-cadherin. Tricin decreased FAK protein levels and suppressed focal-adhesion-kinase (FAK)-downstream-signal activation. Most importantly, tricin dose-dependently upregulated microRNA-7 (miR-7). Transfection with an miR-7 inhibitor suppressed miR-7 expression, increased FAK expression, and promoted the proliferation and invasion in C6 cells. The data support a novel anticancer mechanism of tricin that involves upregulation of FAK-targeting miR-7 in C6 glioma cells.

中文翻译：

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Tricin通过聚焦黏附激酶激酶靶向MicroRNA-7上调抑制C6胶质瘤细胞的增殖和侵袭

Tricin是米糠中大量存在的天然类黄酮，研究了其在C6胶质瘤细胞中表现出抗增殖和抗侵袭的机制。结果表明，用5、10、25和50μM的Tricin处理48 h显着（p<0.05）抑制的细胞数和菌落数分别为134.3±5.5、114.6±2.5、106.3±3.2和57.3±10.2。Tricin还抑制C6细胞的运动性，迁移和侵袭。Tricin改变了细胞骨架的组织，降低了基质金属蛋白酶（MMP）的表达，并上调了E-钙黏着蛋白。Tricin降低了FAK蛋白水平并抑制了粘着斑激酶（FAK）下游信号激活。最重要的是，Tricin剂量依赖性上调了microRNA-7（miR-7）。用miR-7抑制剂转染可抑制miR-7表达，增加FAK表达并促进C6细胞的增殖和侵袭。数据支持Tricin的新型抗癌机制，该机制涉及上调C6胶质瘤细胞中靶向FAK的miR-7。