Surface Protein Protects Brain Tumor Cells from Immune Attack

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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