Poor survival among colorectal cancer patients tied to biomarker CSN6
MD Anderson News Release August 10, 2015
MD Anderson News Release 08/10/2015
A protein called CSN6 has been found to be correlated with poor survival among patients with colorectal cancer, according to a study at .
The study revealed that CSN6, a subunit of a protein complex known as COP9 signalosome, is overexpressed in colorectal cancer tissue samples. The finding could be significant in the search for alternative treatment strategies for colorectal cancer.
¡°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 . ¡°This occurs when CSN6 is deregulated through a series of cellular signaling pathways.¡±
The biomarker is normally regulated through signaling pathways called EGFR and ERK. When CSN6 is overexpressed via ERK2 in particular, however, it can lead to deregulation of another protein, beta-catenin, a transcription factor known to be linked to cancer development.
¡°Our findings indicated that deregulation of CSN6 by ERK2 resulted in stabilization and activation of beta-catenin, which is important for colorectal cancer development,¡± said Lee. ¡°We further defined the mechanism by which beta-catenin is regulated in this cancer.¡±
The team¡¯s study findings were published in the Aug. 10, 2015 issue of .
Currently, the standard treatment for colorectal cancer patients at high risk of developing recurrent or metastatic cancer includes surgery, chemotherapy and targeted therapies.
¡°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.¡±
MD Anderson study members included Lekun Fang, M.D., Hyun Ho Choi, Ph.D. and Enrique Fuentes-Mattei, Ph.D., of Molecular and Cellular Oncology; Sai-ching J. Yeung, M.D., Ph.D., Endocrine Neoplasia and Hormonal Disorders; and David Menter, Ph.D., Gastrointestinal Medical Oncology. Other participating institutions included Sun Yat-sen University, Guangzhou, China; and Academia Sinica, Taipei, Taiwan.
The study was funded by the National Institutes of Health (ROCA089266 and CA16672), the Susan G. Komen Breast Cancer Foundation; the Ministry of Science and Technology of China (2015CB554000); the Program of Introducing Talents of Discipline to Universities (B12003); and the International S&T Cooperation Program of China (2011DFA32570).