A study at The University of Texas MD Anderson Cancer Center, Houston, led by Mong-Hong Lee, PhD, Professor of Molecular and Cellular Oncology, has demonstrated the significance of CSN6 in regulating Myc which may well open up a new pathway for treating and killing tumors. The study results are published in a recent issue of Nature Communications.1
“We have discovered that CSN6 is a strong oncogene that is frequently overexpressed and significantly speeds up tumor growth in many types of cancer,” said Dr. Lee. “Furthermore, CSN6 also affects the expression of Myc in tumors.”
Myc is a proto-oncogene or master cancer gene that spurs tumor growth in a variety of cancers including breast, lung, colon, brain, skin, leukemia, prostate, pancreas, stomach, and bladder.
Dr. Lee said that the study findings are important because targeting Myc is a challenging task due to its unique protein structure. Even though it has been studied for decades, no effective inhibitor for Myc has been successfully developed. His team’s study found that inhibiting CSN6 quickly destabilizes Myc, greatly impairing metastasis and tumor growth.
“This has the potential to unlock a promising and completely new door to effectively eliminating tumors and suppressing cancers that overexpress Myc,” said Dr. Lee. ■
Disclosure: The study was funded by the National Institutes of Health, the Fidelity Foundation, and the Susan G. Komen Breast Cancer Foundation. The authors reported no potential conflicts of interest.
Reference
1. Chen J, et al: CSN6 drives carcinogenesis by positively regulating Myc stability. Nat Commun. November 14, 2014 (early release online).
