Targeting protein may mitigate ovarian cancer cells from spreading

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Washington D.C. [USA]: Preventing a protein from performing its job may keep a certain type of ovarian cancer cell from growing and dividing uncontrollably in the lab, says researcher.

In a study published in the Journal of Molecular Cancer Research, the researchers identified the protein as a potential therapeutic target for high-grade serous ovarian cancer cells.

Approximately 70 per cent of patients with this type of ovarian cancer relapse with the chemo-resistant disease, increasing the need for new approaches to treatment.

Katherine Aird, the other researcher of the study in her lab, has identified a potential method to put high-grade serous ovarian cancer cells in a “sleep state” called senescence.

“One of the biggest problems of cancer cells is they can grow forever without stimulus. By inducing senescence, the cells can no longer divide and grow,” said Aird.

Cells break down and build up the chemicals needed for supporting life through various cycles and pathways in a process known as metabolism.

“A hallmark of cancer cells is that their metabolic processes are often different from normal, healthy cells,” said Erika Dahl, lead author of the paper.

The metabolites in each line of cells were quantified using spectrometry. After comparing differences in their metabolic processes, the lab found that the cancerous cells prefer to use sugars in the citric acid cycle, instead of making lactate, the more common route.

“Many therapies target glycolysis, but that may not be the best approach,” Dahl said. She noted that often when targeting glycolysis, there could be toxic damage to normal, and healthy tissue.

“The Food and Drug Administration has already approved a drug that targets the mutant form of the protein. One of the drugs that target the mutant form can also target the wildtype form. One of our long-term goals is to try and repurpose this already-approved drug as a treatment for this form of ovarian cancer,” Aird said.

The research team has found that inhibiting the wildtype form of the protein may be an effective strategy for future therapies for all stages of high-grade serous ovarian cancer. When these cells spread to other parts of the body, they adopt a form that is different from the original cancer cells.

“It is important that therapies are effective at later stages, as this is when ovarian cancer patients are typically diagnosed,” said Dahl.