New research, published in the journal Genes & Development, makes the case that manipulating elements of cells called nuclear pores could eventually prevent cancerous cells from proliferating.
All cells have nuclear pores, but they appear in excessive numbers in some cancerous cells.
Cancer is the second most common cause of death in the U.S., after heart disease. The American Cancer Society estimate that about 1.7 million cancer cases will be diagnosed in the U.S. in 2018 and more than 600,000 Americans will die from cancer this year.
This translates to about 1,670 cancer-related deaths each day.
All cells have nuclear pores — they are essential transport channels that help to move cellular material to and from a cell's nucleus, which is the part of the cell that contains its genes.
Nuclear pores are an area of interest for cancer research because they appear in excessive numbers in certain cancerous cells. Some research has therefore looked at how nuclear pores affect cancer treatment.
For instance, scientists know from the findings of other studies that preventing cancer-related proteins from passing through nuclear pores can dramatically impact cancer treatment. They also know that nuclear pores can promote treatment resistance in some aggressive cancers, as they can excrete chemotherapy from the cells, weakening its benefits.
Nuclear pores are made up of a type of protein called nucleoporins. The researchers behind the new study, from the Salk Institute for Biological Studies in La Jolla, CA, were particularly interested in a nucleoporin called Tpr, which has previously been associated with some cancers.
Surprising finding: Removing Tpr from cells
The Salk team made some unique findings. Their study is the first to illustrate how each nuclear pore within a cell is different. They also found that when Tpr is removed from a cell, the cell's number of nuclear pores increases.
This was a surprising finding. "Typically, when you 'knock down' or remove some of the proteins that make up the nuclear pore complex, the total number of nuclear pores goes down," explains first author Asako McCloskey.
The researchers say that the dramatic increase in the number of nuclear pores that occurs when Tpr is removed suggests that Tpr contributes to regulating how nuclear pores are assembled. This means that Tpr does not just play a role in the transport of cellular material.
"Previously, we didn't have the tools to artificially increase nuclear pores," says lead author and Salk's vice president and chief science officer, Martin Hetzer.
"Our study provides an experimental avenue to ask critical questions: What are the consequences of boosting the number of nuclear pores in a healthy cell to mimic those found in a cancer cell? Does this affect gene activity? Why do cancer cells increase the number of nuclear pores?"
Hetzer and colleagues are hopeful that these findings could one day lead to a breakthrough treatment that prevents the proliferation of cancer cells by manipulating the numbers of nuclear pores.
They believe that it may also be possible to counteract aggressive cancers' resistance to treatment by preventing nuclear pores from exporting chemotherapy out of the cells.
Recently, Medical News Today reported on another study investigating potential targets for drug-resistant tumors. That study identified a mechanism that promotes cell growth, and it involves a previously unknown protein complex called mammalian target of rapamycin complex 3 (mTORC3).