Open AccessSp5 negatively regulates the proliferation of HCT116 cells by upregulating the transcription of p27
Author(s) -
Masaharu Miyamoto,
Tomoatsu Hayashi,
Yuki Kawasaki,
Tetsu Akiyama
Publication year - 2018
Publication title -
oncology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2018.7793
Subject(s) - wnt signaling pathway , downregulation and upregulation , cell cycle , transcription factor , oncogene , enhancer , cell growth , biology , microbiology and biotechnology , cancer research , signal transduction , cell , gene , genetics
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.