Today, in many places around the world, Halloween celebrations will take place. The spooky holiday culminates with costumes, pumpkins, and trick-or-treating, but its roots go back to an ancient Celtic festival called Samhain. The Celts celebrated Samhain at the same time of year as we celebrate Halloween today, midway between the fall equinox and the winter solstice. The autumn date marked the end of the harvest and the start of the “dark half of the year.”
Some of the spooky aspects of Halloween also stem from Samhain. The Celts believed the barrier between the physical and spiritual worlds broke down during Samhain, allowing humans and spirits to meet. Druid priests led the Samhain celebrations, which included leaving offerings on the outskirts of villages to satisfy the fairies that would venture into the physical world. People also dressed up! However, instead of princesses and firefighters, the Celts dressed as scary animals and monsters to ward off the spirits.
In the spirit (no pun intended) of today’s Halloween celebrations, let’s delve into the mysterious world of “zombie cells”, a resilient subset of cells that do not die easily. Zombie cells are characterized by senescence, a key defensive mechanism that they undergo. Senescence occurs when cells age and cease to divide. But, despite no longer dividing to generate new cells, senescent cells don’t die easily, much like their namesake.
Zombie cells remain ambiguous, so we can’t easily predict their phenotype or classify them as “good” or “bad.” Like many subsets of cells, zombie cells serve different functions depending on their cellular setting.
Cells that become senescent often do so in response to stress, and we know that cancer poses tremendous stresses on cellular and physical levels. In the setting of cancer, senescence protects the cells by reducing their activity and energy demands. This could signify a defense mechanism, by preventing the overgrowth of cells that could become cancer.
Zombie cells can prevent the onset of cancer by inhibiting the replication of pre-malignant cells and thereby preventing them from becoming cancerous. For example, pre-cancerous lumps of cells, known as polyps, can develop in the colon, stomach, or nose. While these cells can remain relatively harmless, they can also develop into cancer. However, cancer genes can flip a switch, forcing dormant zombie cells to overcome senescence and develop into a tumor.
Understanding how pre-cancerous cells enter and exit a senescence state can also provide scientists with promising clues for developing new anti-cancer drugs. One study identified a protein, POU2F2, that facilitates cells in overcoming senescence, which could become a valuable biomarker or treatment target.
Sources: Cancer Cytopathol, Cell Genomic
