Study Finds Endogenous Retroviruses Have a Role in Cancer’s Resilience

Researchers from the University of Colorado Boulder have uncovered a surprising link between ancient viral DNA and cancer's ability to survive and thrive. This research, published in Science Advances, challenges the long-held belief that endogenous retroviruses, remnants of viral infections in our primate ancestors, were merely junk DNA.

The study, led by Edward Chuong, reveals that these viral fragments, which make up about 8% of the human genome, can act as genetic switches, activating nearby genes that promote cancer development and growth.

Focusing on a specific lineage of endogenous retrovirus called LTR10, which infected primates approximately 30 million years ago, the team found high activity levels in several cancer types, including lung and colon cancer. In colorectal cancer patients, LTR10 was active in about one-third of tumors examined.

Using CRISPR gene editing, the researchers demonstrated that silencing these viral sequences could deactivate critical cancer-promoting genes. "We saw that when you silence this retrovirus in cancer cells, it turns off nearby gene expression," said Atma Ivancevic, the study's first author.

The team's experiments extended to mice, where removing an LTR10 "switch" from tumor cells led to the deactivation of key cancer-promoting genes and improved the effectiveness of tumor-shrinking treatments.

Notably, the study suggests that LTR10 activates genes in the MAP-kinase pathway, a cellular pathway often dysregulated in cancers. This finding provides new insight into how existing cancer therapies, such as MAP-kinase inhibitors, may work.

Chuong speculates that as people age, genomic defenses weaken, potentially allowing these ancient viral elements to reawaken and contribute to various health issues. "Endogenous retroviruses are not the whole story, but they could be a big part of it," he concluded.