The Spanish National Cancer Research Centre (CNIO) announced the discovery of a protein called RanBP6 as a regulator of epidural growth factor receptor (EGFR). The study, as originally printed in the journal Nature Communications demonstrated how the silencing of the protein promoted unregulated glioma growth, and EGFR expression was upregulated. The introduction of the RanBP6 protein slowed tumor growth in mice, however. The researchers are convinced that this new information could have significant implication when it treating glioblastoma. Read the the study in Nature Communications or the article on Medical Xpress.
Glioblastoma is a rare cancer that originates in the brain. It is also the most aggressive form of brain cancer. Initial symptoms can include personality changes, headaches, and symptoms similar to a stroke. The cancer often worsens rapidly and patients may lose consciousness. At this juncture, there is no way to prevent the disease, with treatment often involving surgery, chemotherapy, and radiation therapy. However, this cancer form recurs in most cases, and few people live more than fifteen months after diagnosis. Less than three to five percent of people live to five years or beyond. To learn more about this cancer, click here.
EGFR is a critically important factor in normal growth development, but it also plays a role in cancer development as well. Abnormal activation of EGFR is a major cause for stimulating tumor cell growth This abnormal activation is often caused by the shutting off of the RanBP6 protein. This shutting off inhibits the nuclear translocation of another protein, STAT3, which results in the heavy activation of EGFR signaling.
Massimo Squatrito, one of the researchers, is convinced that this new understanding is of essential importance. Currently, STAT3 inhibitors are being investigated as possible treatment option not only for glioblastoma, but for other cancer forms as well. Unfortunately, the information from the study suggests that a side effect of inhibiting STAT3 could be the activation of EGFR, which could actually make the environment more favorable for cancer growth.
It appears that the protein that should be targeted for inhibition should in fact be EGFR, not STAT3; the reconstitution of RanBP6 was shown to reduce tumor growth in a xenograft model using mice, and many patients with the cancer showed focal deletions of the RanBP6 locus.
