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Gene linked to early growth may shape new approaches to cancer research

Hebrew University researchers identify mechanism connecting youth and disease.

The Rothberg International School on the Hebrew University of Jerusalem's Mount Scopus Campus, Aug. 16, 2021. Photo by Gunner Vitaliy Bothman/TPS.
The Rothberg International School on the Hebrew University of Jerusalem’s Mount Scopus Campus. Photo by Gunner Vitaliy Bothman/TPS.

A newly identified gene may help explain why faster growth and early development in youth can come with a trade-off later in life, including increased risk of aging-related diseases and cancer, Israeli scientists announced on Tuesday.

Researchers at the Hebrew University of Jerusalem found that the gene vgll3 plays a central role in accelerating early growth and reproduction, while potentially influencing biological aging processes and disease risk in later life. Researchers say the discovery could eventually help reshape scientific understanding of the biological links between development, aging, and disease.

The vgll3 gene (Vestigial-like family member 3) is a regulatory gene involved in controlling growth and developmental timing across a range of species. It has previously been linked to the timing of puberty and sexual maturation. According to the study, vgll3 is thought to influence pathways related to cell growth, hormone regulation, and tissue development, making it a focus for research into how organisms balance growth, reproduction, and long-term health.

The study was led by an international team including Dr. Eitan Moses, Dr. Marva Bergman and Prof. Itamar Harel of the Hebrew University, in collaboration with researchers from the Technion-Israel Institute of Technology and Britain’s University of East Anglia.

To study the gene, researchers used the African turquoise killifish, a small fish species widely used in aging research because of its short lifespan, which allows scientists to observe aging-related processes in a matter of weeks.

Using CRISPR gene-editing technology, the team altered vgll3 and tracked its effects throughout the fish’s life. The results indicated significant differences: fish with altered vgll3 grew faster and reached sexual maturity earlier than normal, traits that would likely improve reproductive success in the wild.

However, these advantages came with high long-term costs. The same fish had shorter lifespans and developed more age-related diseases, including tumor growth resembling melanoma, a type of skin cancer.

Further analysis showed that vgll3 influences key biological processes, including cell division, stem cell activity, and DNA repair—processes essential for growth, tissue maintenance, and recovery from cellular damage. The study suggests that while these systems are essential in early life, sustained high activity over time may contribute to accumulated damage and disease later in life.

Harel said the findings suggest cancer may be closely tied to the same biological systems that drive healthy development.

“What’s fascinating—and slightly terrifying—is that the cancer we see in these fish isn’t a random accident,” he said. “It’s the direct shadow of their youthful vitality. The same machinery that drives a cell to build a young body is hijacking the system to build a tumor in the old one.”

Because of the vgll3 gene’s overlap with puberty and hormone regulation, the researchers say the findings could help improve understanding of human development and age-related diseases, including cancer, though direct relevance to humans remains uncertain.

However, they emphasize that the research is still early and based on animal models, meaning direct medical applications are not yet available.

Scientists say the next challenge is determining whether it is possible to preserve vgll3’s beneficial effects in early life while reducing its harmful impact later in life. If successful, that line of research could open new approaches to cancer prevention and strategies aimed at extending healthy lifespan.

The study was published in the peer-reviewed journal Nature Communications.

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