The findings could offer a new approach toward combating cancer.

The research team was investigating how the Myc gene promotes cancer growth when it made a surprising discovery: The gene actually increases the utilization of glutamine by cancer cells, according to Chi V. Dang, MD, PhD, a professor of oncology at Johns Hopkins.

Protein experts joined the team effort, searching for proteins that responded to Myc. The researchers examined human cancer cells with the Myc gene turned on or off and found eight proteins in the cell's mitochondria that displayed a distinct response to the gene.

One of the proteins that responded to the Myc gene, glutaminase (GLS), supports the production of cellular energy. Cancer growth slowed down markedly when researchers removed GLS.

Building on earlier research, the team found that the Myc gene did not affect GLS directly, but rather affected an intermediary -- "something that in turn controls GLS," according to Ping Gao, PhD, a research associate in hematology at Johns Hopkins.

That "something" turned out to be some microRNAs, small bits of RNA that can bind to and inhibit RNAs, which contain instructions for making proteins. Two microRNAs called "miR23a" and "miR23b" link Myc to GLS expression.

The scientists intend to continue their exploration in a study with mice to see if removing GLS can impede cancer growth.

"If we know how cancer cells differ from normal cells in how they make energy and use nutrients, we can identify new pathways to target for designing drugs with fewer side effects," said Gao.

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