New anti-cancer drug looks promising in lab

29 Jun

Much of research to beat cancer tends to concentrate on the various genetic mutations

behind different cancers. Now, a new study in the journal Cancer Cell takes a

different approach – it targets the pathways that hungry cancer cells use to satisfy their

voracious appetite for energy.

cancer cells
The drug killed cancer cells by shutting off their two preferred sources of energy without harming healthy cells.

Cancer cells grow fast and divide, and to do this they rely on preferred ways of getting

energy – even if other means are available.

The idea of foiling cancer by undermining the way it uses energy differently to healthy

cells is not new, but it has received more attention lately.

For their study, researchers at Saint Louis University, MO, focused on two metabolic

pathways that senior author Thomas Burris, professor and chair of pharmacology and

physiology, says cancer cells are “addicted to.”

“They need tools to grow fast,” explains Prof. Burris, “and that means they need to have all of the parts

for new cells and they need new energy.”

One pathway that cancer cells use to make the parts they need, is called the Warburg

effect, which ramps up use of glucose, and the other is called lipogenesis, whereby the cells

can make their own fats for rapid growth.

SR9243 shuts off cancer cells’ preferred fat and sugar energy sources

In their study paper, the team explains how a small molecule that selectively targets

these two pathways stopped cancer cell growth in cultured tumor cells in the lab and in human

tumor cells grown in animals without harming healthy tissue or inducing weight loss,

inflammation or liver damage.

The small molecule – called SR9243 – started off as an anticholesterol drug

candidate. The drug targets fat synthesis in cells so they can’t produce their own fat. It

also suppresses abnormal glucose consumption and cuts off cancer cells’ energy


The molecule stops these two processes by turning down the genes that drive them. Denied

their favorite fat and sugar energy sources, the cancer cells cannot make the parts they need

to thrive and die.

The researchers say that because the Warburg effect is not a feature of normal cells and

because most normal cells can get their fat from outside, SR9243 only kills cancer cells and

does not harm healthy cells.

Prof. Burris explains that some cancers are more sensitive to the drug than others:

“It worked very well on lung, prostate and colorectal cancers, and it worked

to a lesser degree in ovarian and pancreatic cancers.”

The team found SR9243 also seems to work on glioblastoma, a type of brain cancer that is

very hard to treat. However, the drug is not able to cross the blood-brain barrier very

effectively, so the challenge will be to find a way to help it to do that.

It also appears that SR9243 can increase the effectiveness of existing chemotherapy drugs

when used in combination with them.

Meanwhile, Medical News Today recently learned how correcting disruption to a

tumor suppressor gene in mice successfully reverted colorectal

cancer cells to normal functioning cells. Within 2 weeks, the tumors regressed and

disappeared, or reintegrated into normal tissue, say researchers writing in the journal


Written by Catharine Paddock PhD