Just like what we need for a harmonious, happy and functioning society, tiny cells in our bodies usually work together, each playing its part and sometimes even sacrificing its own life so that we may exist.
But what if a cell decides to break the rules? Choosing its own survival over ours?
That is where cancer begins. A single cell refusing to die, multiplying endlessly and draining the life out of its neighbours.
This strange betrayal, where a once selfless cell turns selfish, has fascinated me and made me want to understand why.
Sadly, many of us don’t have to look far to see the consequences; we all know someone who has faced, or is facing, this fight.
Breast cancer is one of the most common of these battles, affecting women far more often than men. As we grow older, the risk rises, often beginning quietly, almost unnoticed, in the breast.
But these cells don’t stay put. They wander, nesting in the bones, liver, lungs, or even the brain.
Wherever they go, they bring chaos; stealing nutrients and oxygen, shutting down vital functions and even turning healthy cells to become just as destructive.
Among the different types of breast cancers, one emerges as a supervillain: triple-negative breast cancer or TNBC.
This type of breast cancer is especially aggressive, racing away from where it began with alarming speed. TNBC hijacks the laws that cells normally follow and twists them to its advantage, but it does it with ruthless efficiency.
The tumour grows and spreads rapidly, expertly escaping from the immune cells patrolling and surviving aggressive cancer treatments, only to return later.
Unlike other breast cancers, TNBC cannot be precisely targeted. Its very name, "triple-negative", reflects the three key targets used to treat breast cancer are absent.
This leaves us with treatments like chemotherapy that often feels like forcing open a locked door with a battering ram, effective but destructive, damaging healthy cells along the way. It’s a fight that weakens not just the disease, but the people battling it too.
But what if we could turn the tables? What if we could use the very rules TNBC exploits, and make it slow itself down?
That question is what drives my research. One protein in particular, called CDH11, caught my attention.
CDH11 has multiple roles, but one of its most important roles is acting like Velcro, helping cells stick together but also peel apart when the body needs repair, such as during healing our wounds.
But TNBC cells hijack this helpful mechanism, turning CDH11 from a healing tool into a weapon for spreading cancer cells throughout the body.
What intrigued me further was a discovery that a tiny doorway on the cell surface, allowing for salt to move in or out of cells called ENaC, can actually decrease the amount of CDH11 present in TNBC cells.
Simply put, a doorway that allows for salt to move through restricts TNBC cells from detaching and spreading.
My research builds on this connection. I study how CDH11 behaves in TNBC cells that have a higher-than-normal amount of ENaC, exploring the mechanism through which this small doorway could be the hidden weakness in the most aggressive breast cancer type.
For me, this tiny doorway could help us lead the way for the much-needed key to the locked door, a key to eliminate TNBC cells without destroying the healthy cells around them.
This opens new possibilities to improve the treatment of TNBC. If CDH11 is confirmed as a tool that cancer cells exploit to spread, it could serve as a marker for doctors, helping them predict how likely the cancer is to move beyond the breast.
ENaC, on the other hand, may act as a regulator for CDH11, giving us insight on how aggressive the cancer is, allowing for more personalised treatment plans.
And perhaps in the future, we could design therapies that increase the amount of ENaC only in TNBC cells, forcing the cancer to weaken itself and giving patients gentler, more effective treatment options.
Cancer research moves forward one rule at a time, each discovery showing us how cancer bends or breaks them. If we can learn how to set these rules right again, perhaps we can restore harmony to the very system cancer disrupts.
Not foreign weapons, but tools hidden in plain sight within our body.
■ Nidhi Bhagi is studying for an honours degree in biomedical sciences in the department of physiology/biomedical science, University of Otago.
