To Halt Brain Cancer Hijack, Target Healthy Cells

Cancer treatments should target the cells around a tumor to stop it from spreading, new University of British Columbia research into brain cancer suggests.

Glioma, the most aggressive form of adult brain cancer, is what UBC research team Christian Naus, Wun Chey Sin and John Bechberger specializes in studying. Glioma has a low five-year survival rate of 30 per cent because it is so hard to totally remove cancer cells without compromising brain functions. Chemotherapy and radiotherapy do not prevent the regrowth of remaining cancer cells.

In this new study, the team introduces an alternative route to control the glioma cancer cells. The cancerous cells mingle with astrocytes, a type of cell that regulates the environment in the brain to create favorable conditions for brain functions.

The research team discovered that glioma cells can reprogram the astrocytes with little pieces of genetic code called microRNAs. Those codes function like master switches, turning specific sets of genes on and off.

Naus, a professor in the Department of Cellular & Physiological Sciences in the Life Sciences Institute and an investigator with the Djavad Mowafaghian Centre for Brain Health, said:

“This is the first evidence that microRNA can go from glioma cells into astrocytes and reprogram them to provide an altered environment that stimulates tumor growth and invasion.”

Sin, a research associate leading the glioma investigation in the Naus laboratory, added:

“We should consider the possibility of creating a treatment that would temporarily modify the healthy astrocytes around the tumor so the cancer cells can’t hijack them.”

Astrocytes promote glioma invasion via the gap junction protein connexin43.
Sin WC, Aftab Q, Bechberger JF, Leung JH, Chen H, Naus CC.
Oncogene. 2015 Jul 13. DOI: 10.1038/onc.2015.210. PMID: 26165844

Gap junctions modulate glioma invasion by direct transfer of microRNA.
Hong X, Sin WC, Harris AL, Naus CC.
Oncotarget. 2015 May 4. PMID: 25978028

Reduction in gap junction intercellular communication promotes glioma migration.
Aftab Q, Sin WC, Naus CC.
Oncotarget. 2015 May 10;6(13):11447-64. PMID: 25926558

ITop Image: Oncogene. Basic Research Laboratory, Frederick Cancer Research Facility, National Cancer Institute, National Institutes of Health.