ArticleMolecular cancer2010
The promoter for intestinal cell kinase is head-to-head with F-Box 9 and contains functional sites for TCF7L2 and FOXA factors.
Article in Molecular cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Forkhead box K1 regulates the malignant behavior of gastric cancer by inhibiting autophagy.Annals of translational medicine · 2020Article
- miR-340-FHL2 axis inhibits cell growth and metastasis in ovarian cancer.Cell death & disease · 2019Article
- FOXK1 interaction with FHL2 promotes proliferation, invasion and metastasis in colorectal cancer.Oncogenesis · 2016Article
- Direct regulation of FOXK1 by C-jun promotes proliferation, invasion and metastasis in gastric cancer cells.Cell death & disease · 2016Article
- Intestinal cell kinase is a novel participant in intestinal cell signaling responses to protein malnutrition.PloS one · 2014Article
- Distinct expression patterns of ICK/MAK/MOK protein kinases in the intestine implicate functional diversity.PloS one · 2013Article
- Fibroblast growth factor receptor-3 (FGFR-3) regulates expression of paneth cell lineage-specific genes in intestinal epithelial cells through both TCF4/beta-catenin-dependent and -independent signaling pathways.The Journal of biological chemistry · 2011Article
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4 authors at 2 institutions in 1 country.
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Abstract
backgroundIntestinal cell kinase (ICK; GeneID 22858) is a conserved MAPK and CDK-like kinase that is widely expressed in human tissues. Data from the Cancer Genome Anatomy Project indicated ICK mRNA is increased in cancer, and that its expression correlated with expression of mRNA for an uncharacterized F-box protein, FBX9 (GeneID: 26268). ICK and FBX9 genes are arranged head-to-head on opposite strands, with start sites for transcription separated by approximately 3.3 kb. We hypothesized ICK and FBX9 are potentially important genes in cancer controlled by a bidirectional promoter.
resultsWe assessed promoter activity of the intergenic region in both orientations in cancer cell lines derived from breast (AU565, SKBR3), colon (HCT-15, KM12), and stomach (AGS) cancers, as well as in embryonic human kidney (HEK293T) cells. The intergenic segment was active in both orientations in all of these lines, and ICK promoter activity was greater than FBX9 promoter activity. Results from deletions and truncations defined a minimal promoter for ICK, and revealed that repressors and enhancers differentially regulate ICK versus FBX9 promoter activity. The ICK promoter contains consensus motifs for several FOX-family transcription factors that align when mouse and human are compared using EMBOSS. FOXA1 and FOXA2 increase luciferase activity of a minimal promoter 10-20 fold in HEK293T cells. Consensus sites for TCF7L2 (TCF4) (Gene Id: 6934) are also present in both mouse and human. The expression of beta-catenin increased activity of the minimal promoter approximately 10 fold. ICK reference mRNAs (NM_014920.3, NM_016513) are expressed in low copy number and increased in some breast cancers, using a ten base tag 5'-TCAACCTTAT-3' specific for both ICK transcripts.
conclusionICK and FBX9 are divergently transcribed from a bidirectional promoter that is GC-rich and contains a CpG island. A minimal promoter for ICK contains functional sites for beta-catenin/TCF7L2 and FOXA. These data are consistent with functions that have been proposed for ICK in development and in proliferation or survival of some breast and colon cancers.
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