An MD Anderson study has found that a protein called CSN6 is linked to poor survival among patients with colorectal cancer.
The study, published in the Aug. 10 issue of Cancer Cell, revealed that CSN6, a subunit of a protein complex known as COP9 signalsome, is overabundant in colorectal cancer tissue samples.
The finding could be significant in the search for alternative treatment options for colorectal cancer patients.
“CSN6 is a biomarker that is elevated in colon cancer and leads to worse recurrence-free survival,” said Mong-Hong Lee, Ph.D., professor of Molecular and Cellular Oncology. “This occurs when CSN6 is deregulated through a series of cellular signaling pathways.”
Normally regulated through signaling pathways called EGFR and ERK, the biomarker is overexpressed via ERK2 and can lead to deregulation of another protein, beta-catenin, a known link to colorectal cancer development.
The findings indicate that deregulation of CSN6 by ERK2 results in stabilization and activation of beta-catenin, leading to colorectal cancer development.
“The molecular alterations in colorectal cancer have been studied extensively,” said Lee. “However, a more detailed picture of the pathways deregulated in this cancer has yet to emerge. Defining those molecular alterations can help guide treatment and improve clinical care.”
Currently, the standard recommended treatment for colorectal cancer patients is at high risk of developing recurrent or metastatic cancer includes surgery, chemotherapy, and targeted therapies. With the findings of this latest research, scientists are now one step closer to developing new strategies to fight the disease.
Read the full press release here.