Transcriptome variations in human CaCo-2 cells: a model for enterocyte differentiation and its link to iron absorption
Complete clinical expression of the HFE1 hemochromatosis is very likely modulated by genes linked to duodenal iron absorption, whose level is conditioned by unknown processes taking place during enterocyte differentiation. We carried out a transcriptomic study on CaCo-2 cells used as a model of ente...
Saved in:
Published in: | Genomics (San Diego, Calif.) Vol. 83; no. 5; pp. 772 - 789 |
---|---|
Main Authors: | , , , , , , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
San Diego, CA
Elsevier Inc
01-05-2004
Elsevier |
Subjects: | |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | Complete clinical expression of the HFE1 hemochromatosis is very likely modulated by genes linked to duodenal iron absorption, whose level is conditioned by unknown processes taking place during enterocyte differentiation. We carried out a transcriptomic study on CaCo-2 cells used as a model of enterocyte differentiation in vitro. Of the 720 genes on the microarrays, 80, 50, and 56 were significantly down-regulated up-regulated, and invariant during differentiation. With regard to iron metabolism, we showed that
HEPH,
SLC11A2,
SLC11A3, and
TF are significantly up-regulated, while
ATP7B and
SLC39A1 (and
SFT) are down-regulated and
ACO1,
dCYTb,
FECH, and
FTH1 show constant expression. Ontological annotations highlight the decrease in the expression of cell cycle and DNA metabolism associated genes as well as transcription, protein metabolism, signal transduction, and nucleocytoplasmic transport associated genes, whereas there are increases in the expression of genes linked to cell adhesion, lipid and xenobiotic metabolism, iron transport and homeostasis, and immune response. |
---|---|
Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0888-7543 1089-8646 |
DOI: | 10.1016/j.ygeno.2003.11.014 |