Cancer is a devastating disease and is the second leading cause of death in the U.S. One of the hallmarks of cancer is genomic instability, or the tendency to accumulate mutations and damage to the DNA that leads to genome alterations during cell division. DNA mutations can arise from exposure to ultraviolet or X-ray radiation or from certain chemicals known as carcinogens; however, our cells have developed mechanisms to monitor and repair damaged DNA. Stability of the genome can also be threatened by the translation of certain messenger RNAs (mRNA). mRNA, copied from DNA, serves as the genetic code for the building of proteins. Certain mRNAs are known to be associated with cancer metastasis. To counteract this threat, a specific protein, heterogenous nuclear ribonucleoprotein E1 (hnRNP E1), a tumor suppressor protein, binds these mRNAs and prevents them from making proteins. Researchers at the Medical University of South Carolina (MUSC) have previously demonstrated how hnRNP E1 binds to metastatic-associated RNAs to inhibit their translation. hnRNP E1 binds RNA in the cytoplasm of the cell, but the protein can also be found in the cell’s nucleus. This led researchers to hypothesize that hnRNP E1 might also interact with DNA. Their results, published online on July 16, 2021 in Life Science Alliance, describe a novel role for hnRNP E1 in binding DNA in the nucleus. The open-access article is titled “Heterogeneous Nuclear Ribonucleoprotein E1 Binds Polycytosine DNA and Monitors Genome Integrity.”