Journal
BIOLOGICAL & PHARMACEUTICAL BULLETIN
Volume 40, Issue 5, Pages 733-737Publisher
PHARMACEUTICAL SOC JAPAN
DOI: 10.1248/bpb.b17-00064
Keywords
beta 4-galactosyltransferase 4; transcriptional mechanism; colon cancer; transcription factor; Specificity protein I (Spl)
Categories
Funding
- Ministry of Education, Culture, Sports, Science and Technology of Japan [15K07924]
- Grants-in-Aid for Scientific Research [15K07924] Funding Source: KAKEN
Ask authors/readers for more resources
Increased expression of beta 4-galactosyltransferase (beta 4GalT) 4 has been shown to be associated with meta-static ability and poor prognosis of colon cancer cells. To solve the up-regulation of beta 4GalT4 in colon cancer cells at transcriptional level, we examined the transcriptional mechanism of the beta 4GalT4 gene in SW480 human colon cancer cell line. Luciferase assay using the deletion constructs revealed that the promoter activity of the beta 4GalT4 gene is associated with the region between nucleotides -122 and -55 relative to the transcriptional start site, which contained one Specificity protein 1 (Spl)-binding site. The mutation into the Spl-binding site resulted in dramatic decreased promoter activity. Meanwhile, ectopic Spl expression stimulated the promoter activity significantly. The present study suggests that the expression of the beta 4GalT4 gene is controlled by Spl, and Spl plays a key role in the activation of the beta 4GalT4 gene in colon cancer cells.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available