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A multinational research team discovered a human cell evolutionary arms race mechanism. The discoveries reveal how mobile DNA components hijack cellular activities and how cells might protect themselves to avoid tumors and chronic inflammation.
The research revealed how the LINE1 retrotransposon uses a cell protein to become active in cancers. The researchers also discovered the cell’s protective mechanisms against tumors and chronic inflammation. The findings were published in Nature Communications.
Secret Service agents who live inconspicuously for years before being activated are called “sleepers” by their superiors. The human genome has countless of sleepers known as retrotransposons. These, likely leftovers from viral attacks millions of years ago, have little information to leap out of the genome and replicate. To achieve this, they exploit human cell enzymes.
LINE1, the most common of these sleepers, occurs in about 20% of the genome. Active LINE1 copies and reintegrates into the genetic material at a new position, altering the cell’s design. This may contribute to genomic diversity, but it can become unmanageable, particularly in advancing cancers.
Additionally, activated LINE1 might signal the cell’s immune system, causing chronic inflammation. Thus, human cells have evolved several methods to inhibit its activation. LINE1 mobilization has been poorly understood till recently.
Researchers have discovered how this works: The cell’s non-working protein NRBP1 is recruited by LINE1. This previous kinase lost its enzymatic activities due to gene mutations. LINE1’s uncontrolled replication is a huge concern for the host cell; therefore, it developed a counter-mechanism. NRBP2, a slightly modified duplicate of this protein, labels NRBP1 as trash and disposes of it.
To avoid harm, NRBP2 must defeat NRBP1. Both variables have been seen in cancer biology owing to their diverse roles in tumors, but their functions were unknown. An examination of this competition’s evolutionary history suggests that NRBP2 gained its blocking role later to avoid NRBP1 and LINE1’s damaging effect.
NRBP1 and NRBP2 are not just involved in human tumor growth. They also offer regulatory elements from gene duplication during evolution.
Sources:
Wei Yang et al. (2025). Opposing roles of pseudokinases NRBP1 and NRBP2 in regulating L1 retrotransposition, Nature Communications. DOI: 10.1038/s41467-025-61626-z
How the genome defends itself against internal enemies. https://phys.org/news/2025-07-genome-defends-internal-enemies.html
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