Ancient viral DNA helps embryonic stem cells grow—and cancer hijacks the same switch
Three years ago, George Kassiotis and his team made an unexpected discovery: A specific way of producing a protein called calbindin was found to help cancer cells survive by preventing them from aging. This left Kassiotis, who runs the Crick's Retroviral Immunology Laboratory, confused. Why would a mechanism that boosts cancer growth exist in the first place?
In 2023, scientists George Kassiotis and his team at the Crick Institute made an unexpected discovery while studying cancer cells. They found that a specific protein called calbindin, which helps prevent aging in cancer cells, was switched on by a remnant of ancient viral DNA embedded in our genome. This ancient DNA, called a human endogenous retrovirus (HERV), is not infectious but has retained a function within our cells over time.
Further research revealed that this HERV-calbindin switch was also active in early embryonic stem cells, suggesting its role in development. Researchers Judith Pape and Kathy Niakan collaborated to investigate the impact of removing the HERVH driving the calbindin switch specifically in human embryonic stem cells. Their findings, published in Science Advances, showed that the absence of calbindin led to unhealthy cells that either failed to grow or prematurely differentiated into certain cell types.
The researchers further demonstrated that this HERVH-calbindin pathway is crucial for the proper formation of blastoids, which are models that mimic the early embryonic stage called the blastocyst. Without calbindin, blastoids could not develop correctly, indicating its importance in embryonic development and implantation in the uterus.
This discovery also revealed that cancer cells can exploit the same calcium-regulating pathway to avoid senescence and survive. The researchers propose that targeting the HERVH-calbindin pathway could potentially be a new approach to cancer treatment, allowing the body to maintain its natural anti-aging mechanism while preventing cancer cells from benefiting from it.
Interestingly, this HERVH was integrated into our genome after the split of great apes, including humans, from orangutans around 13 million years ago. This evolutionary trade-off suggests that we have been rewarded with a beneficial genetic instruction that outweighs the risk of cancer cells utilizing the same pathway.
In the future, researchers could explore the potential of HERVH-calbindin as a biomarker for embryo health in fertility treatments, as embryos with this protein are more likely to develop efficiently. Additionally, investigating the role of HERVH-calbindin during and after implantation could provide further insights into early embryogenesis.
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