Selenite Supplementation Decreases Expression of MAZ in HT29 Human Colon Adenocarcinoma Cells

Low dietary intake of the essential trace element selenium can increase the risk of colon cancer. Utilizing RNA arbitrarily primed polymerase chain reaction (RAP-PCR), we sought to identify genes differentially expressed in HT29 human colon adenocarcinoma cells cultured with or without supplemental sodium selenite. One cDNA fragment, present at lower levels in samples from cells supplemented with selenite, had 97% nucleotide sequence identity with a sequence from the 3'-untranslated region of myc-associated zinc-finger protein (MAZ) cDNA. Northern blot analysis showed that steady-state levels of mRNA detected using this fragment as a probe were three times greater in unsupplemented (Se-) than in supplemented (Se+) samples. When a duplicate Northern blot was probed with a 300-bp fragment from the open reading frame of an MAZ cDNA clone, signal intensity was 2.2 times greater in Se- than in Se+ lanes. The MAZ protein has been shown to be a transcription regulator of the c-myc protooncogene. Signal intensity on a Northern blot probed with a segment of c-myc Exon 1 cDNA was 94% greater in Se- than in Se+ lanes. These findings are consistent with the established role for MAZ in regulating c-myc gene expression. They also suggest a molecular mechanism by which selenium intake may affect risk of colon cancer.