It’s been known for a while that nickel-based compounds are linked to cancer. In fact, if we had a Nickel for every time we hear about how dangerous nickel exposure is, well, we might be able to buy a cup of coffee (Nickels just aren’t worth what they used to be!). But the point is, new research is now focusing on the epigenetic “how” behind the high health costs of nickel compounds.
A study conducted by investigators at the NYU School of Medicine aimed to uncover the mechanism that causes exposure to nickel compounds to be so harmful. In previous experiments they had shown a global increase in H3K4 trimethylation, a mark that activates transcription, in A549 cells treated with NiCl2.
Now the researchers wanted to take a closer look. Armed with both ChIP-seq and RNA-seq experimental data, the team matched up H3K4me3 peaks within 5kb of Transcription Start Sites (TSS) for genes highly induced by nickel exposure. Informatic analysis showed that in A549 cells, the top nickel-induced genes also had elevated levels of H3K4me3 throughout their promoter and coding regions.
The NYU group’s work gives new insights into the mechanism that connects nickel compounds to the increased expression of certain genes and subsequent carcinogenesis. Much like another article we’ve featured on formaldehyde toxins, this report also adds to the growing amount of evidence about how our environment can alter epigenetic regulation.
Check out the entire article, it’ll be worth every nickel at PLoS One, April 2011.