Recent data have linked hypoxia, a classic feature of the tumor 
microenvironment, to the function of specific microRNAs (miRNAs); however, 
whether hypoxia affects other types of noncoding transcripts is currently 
unknown. Starting from a genome-wide expression profiling, we demonstrate for 
the first time a functional link between oxygen deprivation and the modulation 
of long noncoding transcripts from ultraconserved regions, termed 
transcribed-ultraconserved regions (T-UCRs). Interestingly, several 
hypoxia-upregulated T-UCRs, henceforth named 'hypoxia-induced noncoding 
ultraconserved transcripts' (HINCUTs), are also overexpressed in clinical 
samples from colon cancer patients. We show that these T-UCRs are predominantly 
nuclear and that the hypoxia-inducible factor (HIF) is at least partly 
responsible for the induction of several members of this group. One specific 
HINCUT, uc.475 (or HINCUT-1) is part of a retained intron of the host 
protein-coding gene, O-linked N-acetylglucosamine transferase, which is 
overexpressed in epithelial cancer types. Consistent with the hypothesis that 
T-UCRs have important function in tumor formation, HINCUT-1 supports cell 
proliferation specifically under hypoxic conditions and may be critical for 
optimal O-GlcNAcylation of proteins when oxygen tension is limiting. Our data 
gives a first glimpse of a novel functional hypoxic network comprising 
protein-coding transcripts and noncoding RNAs (ncRNAs) from the T-UCRs category.