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New York, NY – In a groundbreaking study, scientists at New York University have uncovered a surprising cooperative behavior among cancer cells, revealing a potential new avenue for cancer treatment. Researchers found that cancer cells, contrary to the long-held belief of purely competitive behavior, work together to source vital nutrients from their environment, particularly under stress.
The study, published in the prestigious journal Nature, highlights that when faced with nutrient scarcity, cancer cells engage in a cooperative process to acquire amino acids, essential for their growth and survival. “We identified cooperative interactions among cancer cells that allow them to proliferate,” said Carlos Carmona-Fontaine, an associate professor of biology at NYU and the senior author of the study. “Thinking about the mechanisms that tumor cells exploit can inform future therapies.”
Traditionally, cancer research has focused on the competitive nature of cancer cells, where the strongest cells dominate and tumors become increasingly aggressive. However, the NYU team observed that under nutrient-deprived conditions, cancer cells release an enzyme, CNDP2, which breaks down oligopeptides (small protein fragments) into free amino acids outside the cell. This creates a shared pool of nutrients, benefiting the entire cell population.
“Surprisingly, we observed that limiting amino acids benefited larger cell populations, but not sparse ones, suggesting that this is a cooperative process that depends on population density,” explained Carmona-Fontaine. “It became really clear that there was true cooperation among tumor cells.”
To validate their findings, the researchers used CRISPR gene editing to delete the Cndp2 gene in tumor cells, effectively preventing the production of the CNDP2 enzyme. They found that tumors formed by these modified cells grew significantly slower in mice, especially when combined with diets low in amino acids.
Furthermore, the team tested the drug bestatin, which inhibits CNDP2. When applied to cancer cells, it prevented them from utilizing oligopeptides, leading to cell extinction. This suggests that targeting CNDP2 could be a promising therapeutic strategy.
“Because we’ve removed their ability to secrete the enzyme and to use the oligopeptides in their environment, cells without CNDP2 can no longer cooperate, which prevents tumor growth,” said Carmona-Fontaine.
The researchers believe that their discovery could lead to more targeted and effective cancer treatments. Bestatin, for example, has been used in humans as an adjunct to chemotherapy but has shown limited efficacy on its own. The new findings may help optimize its use or inspire the development of novel drugs.
“We hope that a clearer understanding of this mechanism can help us make drugs more targeted and more effective,” Carmona-Fontaine concluded.
Disclaimer: This article is based on a research study and is intended for informational purposes only. The findings discussed are preliminary and require further research and clinical trials before they can be applied to patient care. Readers should consult with healthcare professionals for medical advice and treatment.
