University Of Minnesota Researchers Find Master Regulator Of Cancer Gene
Researchers at the University of Minnesota’s Masonic Cancer Center have found that the MYC gene, which is key in the development of cancer, partners with a non-coding RNA, PVT1, in turn fueling the growth of cancer cells. This new discovery could help researchers to better understand the relationship between how the MYC gene boosts the development of cancer and in turn, fuel new drug discoveries.
Anindya Bagchi, PhD, assistant professor at UM’s Medical School, and the study’s lead author, commented on the results of the research. “We knew MYC amplifications cause cancer. But we also know that MYC does not amplify alone. It often pairs with adjacent chromosomal regions. We wanted to know if the neighboring genes played a role,” said Bagchi. “We took a chance and were surprised to find this unexpected and counter-intuitive partnership between MYC and its neighbor, PVT1. Not only do these genes amplify together, PVT1 helps boost the MYC protein's ability to carry out its dangerous activities in the cell.”
The researchers found that MYC did not work alone in spreading cancer, as previously believed. Through the use of chromosome engineering, the researchers discovered that there was only cancer growth when strains of MYC and PVT1 were paired up. The researchers stated that better understanding this cycle will help them to uncouple the pair, which could limit cancer growth. The uncoupling process could make a significant impact in the development of treatment for cancer, as it is estimated that MYC is responsible for as many as 20 percent of cancers.
Bagchi elaborated upon the next steps for the research team. “Two major areas present themselves now for research: will breaking the nexus between MYC and PVT1 perform the same in any MYC-driven cancer, even those not driven by this specific genetic location? And how is PVT1 stabilizing or boosting MYC within the cells? This relationship will be a key to developing any drugs to target this mechanism,” Bagchi said.