Treatment of ErbB2-overexpressing BT474 and MDA-MB-453 breast cancer cells with 1 to 10 μmol/L betulinic acid inhibited cell growth, induced apoptosis, downregulated specificity protein (Sp) transcription factors Sp1, Sp3, and Sp4, and decreased expression of ErbB2. Individual or combined knockdown of Sp1, Sp3, Sp4 by RNA interference also decreased expression of ErbB2 and this response was because of repression of YY1, an Sp-regulated gene. Betulinic acid-dependent repression of Sp1, Sp3, Sp4, and Sp-regulated genes was due, in part, to induction of the Sp repressor ZBTB10 and downregulation of microRNA-27a (miR-27a), which constitutively inhibits ZBTB10 expression, and we show for the first time that the effects of betulinic acid on the miR-27a:ZBTB10-Sp transcription factor axis were cannabinoid 1 (CB1) and CB2 receptor-dependent, thus identifying a new cellular target for this anticancer agent.

译文

:用1至10μmol/ L的桦木酸处理过表达ErbB2的BT474和MDA-MB-453乳腺癌细胞抑制细胞生长,诱导细胞凋亡,下调特异性蛋白(Sp)转录因子Sp1,Sp3和Sp4并降低表达的ErbB2。 RNA干扰对Sp1,Sp3,Sp4的单独或组合敲低也降低了ErbB2的表达,这种反应是由于抑制了Sp调控的基因YY1。苯丙酸对Sp1,Sp3,Sp4和Sp调控基因的抑制部分归因于Sp阻遏物ZBTB10的诱导和microRNA-27a(miR-27a)的下调,后者构成性地抑制了ZBTB10的表达,我们首次表明,桦木酸对miR-27a:ZBTB10-Sp转录因子轴的影响是大麻素1(CB1)和CB2受体依赖性的,从而确定了该抗癌剂的新细胞靶标。

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