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Surface Protein Protects Brain Tumor Cells from Immune Attack

By BiotechDaily International staff writers
Posted on 19 Aug 2014
Image: In mice whose brain tumor cells (in green) could not make galectin-1, the body’s immune system was able to recognize and attack the cells, causing them to die. In this microscope image, the orange areas show where tumor cells had died in just the first three days after the tumor was implanted in the brain. Six days later, the tumor had been eradicated (Photo courtesy of the University of Michigan).
Image: In mice whose brain tumor cells (in green) could not make galectin-1, the body’s immune system was able to recognize and attack the cells, causing them to die. In this microscope image, the orange areas show where tumor cells had died in just the first three days after the tumor was implanted in the brain. Six days later, the tumor had been eradicated (Photo courtesy of the University of Michigan).
Malignant glioma brain tumor cells suppress the natural killer cell (NK) immune response by over expressing the surface protein galectin-1, and suppression of this protein renders the tumor cells susceptible to destruction by the immune system.

Galectin-1 (LGALS1 lectin, galactoside-binding, soluble, 1) is a member of the galectin family of beta-galactoside-binding proteins, which has been implicated in modulating cell-cell and cell-matrix interactions. This protein may act as an autocrine negative growth factor that regulates cell proliferation. Autocrine signaling is a form of cell signaling in which a cell secretes a hormone or chemical messenger (called the autocrine agent) that binds to autocrine receptors on that same cell, leading to changes in the cell.

Investigators at the University of Michigan (Ann Arbor, USA) had been studying gliomas, which make up about 80% of all malignant brain tumors, including anaplastic oligodendrogliomas, anaplastic astrocytomas, and glioblastoma multiforme.

In the current study, they used rodent models to demonstrate that malignant glioma cells suppressed NK immune surveillance by over expressing galectin-1. Conversely, galectin-1 deficient glioma cells could be eradicated by host NK cells prior to the initiation of an anti-tumor T-cell response. Results of in vitro experiments published in the July 18, 2014, online edition of the journal Cancer Research demonstrated that galectin-1 deficient GL26-Cit glioma cells were nearly three times more sensitive to NK-mediated tumor lysis than galectin-1 expressing cells.

“This is an incredibly novel and exciting development, and shows that in science we must always be open-minded and go where the science takes us; no matter where we thought we wanted to go,” said senior author Dr. Pedro Lowenstein, professor of neurosurgery at the University of Michigan. “In this case, we found that over-expression of galectin-1 inhibits the innate immune system, and this allows the tumor to grow enough to evade any possible effective T-cell response. By the time it is detected, the battle is already lost.”

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