Miyamoto Masaya, Hayashi Tomoatsu, Kawasaki Yoshihiro, Akiyama Tetsu
Laboratory of Molecular and Genetic Information, Institute of Molecular and Cellular Biosciences, The University of Tokyo, Tokyo 113-0032, Japan.
Oncol Lett. 2018 Mar;15(3):4005-4009. doi: 10.3892/ol.2018.7793. Epub 2018 Jan 15.
The Wnt signaling pathway is aberrantly activated in the majority of human colorectal tumors. β-catenin, a key component of the Wnt signaling pathway, interacts with the T-cell factor/lymphoid enhancer-binding factor family of transcription factors and activates transcription of Wnt target genes. Sp5 is one of the Wnt target genes, and its expression is commonly upregulated in colon cancer cells. The present study demonstrates that the expression of Sp5 is not upregulated in the colon cancer cell line HCT116, in which Wnt signaling is constitutively activated. Furthermore, the results demonstrate that Sp5 has the potential to inhibit cell proliferation through upregulation of the cell cycle inhibitor p27. These findings suggest that HCT116 cells downregulate Sp5 to avoid p27-mediated growth arrest.
Wnt信号通路在大多数人类结肠肿瘤中被异常激活。β-连环蛋白是Wnt信号通路的关键组成部分,它与转录因子T细胞因子/淋巴增强子结合因子家族相互作用,并激活Wnt靶基因的转录。Sp5是Wnt靶基因之一,其表达在结肠癌细胞中通常上调。本研究表明,在Wnt信号被持续激活的结肠癌细胞系HCT116中,Sp5的表达并未上调。此外,结果表明Sp5具有通过上调细胞周期抑制剂p27来抑制细胞增殖的潜力。这些发现表明,HCT116细胞下调Sp5以避免p27介导的生长停滞。