In a new study, researchers have identified a key protein that supports the growth of many colorectal cancers.
The findings reveal that a protein called Importin-11 transports the cancer-causing protein βcatenin into the nucleus of colon cancer cells, where it can drive cell proliferation.
Inhibiting this transport step could block the growth of most colorectal tumors caused by the protein.
The research was conducted by a team at the University of Toronto.
Around 80% of colorectal cancers are associated with mutations in a gene called APC that result in elevated levels of the βcatenin protein.
This increase in βcatenin is followed by the protein’s accumulation in the cell nucleus, where it can activate numerous genes that drive cell proliferation and promote the growth and maintenance of colorectal tumors.
But how βcatenin enters the cell nucleus after its levels rise is poorly understood.
Using CRISPR DNA editing technology, the team developed a new technique that allowed them to screen the human genome for genes that support βcatenin’s activity in colorectal cancer cells.
One of the main genes they identified was IPO11, which encodes a protein called Importin-11 that is known to be involved in nuclear import.
The team found that Importin-11 binds to βcatenin and escorts it into the nucleus of colorectal cancer cells.
Removing Importin-11 from these cells prevented βcatenin from entering the nucleus and activating its target genes.
The researchers discovered that Importin-11 levels are often elevated in human colon cancers.
Moreover, removing Importin-11 inhibited the growth of tumors formed by APC mutant cancer cells isolated from patients.
The team concluded that Importin-11 is required for the growth of colorectal cancer cells.
This finding may help researchers develop new therapies that block this process and reduce the growth of colorectal cancer.
One author of the study is Stephane Angers, a professor in the Department of Pharmaceutical Sciences.
The study is published in the Journal of Cell Biology.
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