By targeting a trait of cancer cell metabolism, a new study conducted at Saint Louis University has found a way to stop cancer cell growth.
Cancer cells prefer to use glucose as fuel even if they have plenty of other resources available and this preference for using glucose as fuel is called the Warburg effect, or glycolysis.
"Cancer cells look for metabolic pathways to find the parts to grow and divide. If they don't have the parts, they just die," said Thomas Burris, chair of pharmacology and physiology at Saint Louis University, US.
Burris and his colleagues created a class of compounds, SR9243, that affect a receptor that regulates fat synthesis. The new compound, which started as an anti-cholesterol drug candidate, turns down fat synthesis so that cells can't produce their own fat.
This also impacts the Warburg pathway, turning cancer cells into more normal cells. SR9243 suppresses abnormal glucose consumption and cuts off cancer cells' energy supply.
When cancer cells don't get the parts they need to reproduce through glucose or fat, they simply die. The drug also has a good safety profile; it is effective without causing weight loss, liver toxicity, or inflammation.
So far, SR9243 has been tested in cultured cancer cells and in human tumor cells grown in animal models. Because the Warburg pathway is a feature of almost every kind of cancer, researchers are testing it on a number of different cancer models.
"It worked very well on lung, prostate, and colorectal cancers, and it worked to a lesser degree in ovarian and pancreatic cancers," Burris said.
The study appeared in Cancer Cell