Shiota Masaki, Izumi Hiroto, Onitsuka Takamitsu, Miyamoto Naoya, Kashiwagi Eiji, Kidani Akihiko, Yokomizo Akira, Naito Seiji, Kohno Kimitoshi
Department of Molecular Biology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
Cancer Res. 2008 Jan 1;68(1):98-105. doi: 10.1158/0008-5472.CAN-07-2981.
YB-1 controls gene expression through both transcriptional and translational mechanisms and is involved in various biological activities such as brain development, chemoresistance, and tumor progression. We have previously shown that YB-1 is overexpressed in cisplatin-resistant cells and is involved in resistance against DNA-damaging agents. Structural analysis of the YB-1 promoter reveals that several E-boxes may participate in the regulation of YB-1 expression. Here, we show that the E-box-binding transcription factor Twist is overexpressed in cisplatin-resistant cells and that YB-1 is a target gene of Twist. Silencing of either Twist or YB-1 expression induces G(1) phase cell cycle arrest of tumor cell growth. Significantly, reexpression of YB-1 led to increase colony formation when Twist expression was down-regulated by small interfering RNA. However, cotransfection of Twist expression plasmid could not increase colony formation when YB-1 expression was down-regulated. Collectively, these data suggest that YB-1 is a major downstream target of Twist. Both YB-1 and Twist expression could induce tumor progression, promoting cell growth and driving oncogenesis in various cancers. Thus, both YB-1 and Twist may represent promising molecular targets for cancer therapy.
YB-1通过转录和翻译机制控制基因表达,并参与多种生物学活动,如大脑发育、化疗耐药性和肿瘤进展。我们之前已经表明,YB-1在顺铂耐药细胞中过表达,并参与对DNA损伤剂的耐药性。YB-1启动子的结构分析表明,几个E盒可能参与YB-1表达的调控。在此,我们表明E盒结合转录因子Twist在顺铂耐药细胞中过表达,且YB-1是Twist的靶基因。沉默Twist或YB-1的表达会诱导肿瘤细胞生长的G1期细胞周期停滞。重要的是,当Twist表达被小干扰RNA下调时,YB-1的重新表达导致集落形成增加。然而,当YB-1表达下调时,共转染Twist表达质粒并不能增加集落形成。总体而言,这些数据表明YB-1是Twist的主要下游靶标。YB-1和Twist的表达均可诱导肿瘤进展,促进细胞生长并推动各种癌症的肿瘤发生。因此,YB-1和Twist都可能是癌症治疗有前景的分子靶标。