An enzyme key to the survival and spread of glioblastoma cancer has been identified by a team of multicenter researchers. Since this enzyme is absent in healthy brain cells, it presents a promising target for ant-cancer drugs.
“The discovery of this may have opened a way to ensure that these cancer cells do not turn as aggressive,” says Alfredo Quinones-Hinojosa, M.D., professor of neurological surgery and oncology at the Johns Hopkins University School of Medicine. Glioblastoma is the most devastating of all human cancers and patients very rarely make it past 14 months after diagnosis. “The latest findings show us a way to starving the cancer cells of the energy they need to grow.”
Many other cancers have an enzyme named glucose-6-phosphatase (G6PC), which enables the diseased cells top devour glucose 200 times faster than do the normal, healthy cells. However, so far there was nothing to suggest that this enzyme was present in glioblastoma. Because Hinojosa was certain that it was in his patients’ tumors, his team set out to study glioblastoma cells from patients.
“Cancer need energy to proliferate much like normal cells” says Sara Abbadi, Ph.D, a research fellow on the team. “But cancer cells are able to survive in conditions where normal, healthy cells cannot.” This is the reason why glioblastoma is so difficult to treat.
When G6PC production is inhibited the viability of the cells and also their mobility is reduced, the team observed. Also, when the team subjected glioblastoma cells with 2DG, a form of glucose that transforms glioblastoma cells into a less malignant form making them sensitive to other treatments, they saw that the cells with uninhibited G6PC production were able to recover their malignancy and could move even faster than they had before. Dual treatment with 2DG and blocking G6PC expression, however, not only prevented those cells from recovering their malignancy but also killed them.
“Part of the problem in treating cancer is that it’s going to be virtually impossible to find one magic bullet,” says Quinones-Hinojosa, “but at least we’re beginning to dismantle the different mechanisms that these cells use.”