Potential Glioblastoma Treatment Shows Promise in Slowing Tumor Recurrence

Updated June 06, 2025
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A⁤ molecule⁤ designed in a virginia Tech lab may offer a new ‍approach to slowing the recurrence⁢ of⁣ glioblastoma, a especially aggressive form of ‍brain cancer. Researchers at the‍ Fralin Biomedical Research Institute at VTC have been studying the molecule extensively.

Published in ⁣ Cell‍ Death and Disease, a study details how the experimental drug, known as JM2, targets ⁢cancer ⁤cells that can renew and regrow even ⁢after chemotherapy and radiation, representing a⁣ potential breakthrough in glioblastoma treatment. Glioblastoma ⁤is the ‍most common malignant brain tumor, with a median survival rate of just over 14 months after diagnosis.

Standard⁢ treatment involves surgery, radiation, ⁢and chemotherapy using temozolomide. Though, the cancer invariably returns as of treatment-resistant glioblastoma stem cells. These cells survive ⁢standard⁤ therapies, leading to tumor regrowth.

Samy Lamouille,assistant⁢ professor ⁣at the Fralin⁢ Biomedical Research Institute and corresponding author of⁣ the study,noted the ability of glioblastoma stem ⁢cells ⁤to ⁤adapt to their ⁤environment and treatment. “These cells can lie dormant, and at some point, they reawaken and ‍then⁤ rebuild the tumor. It’s ⁢critical ⁤to find a way to target this population of cancer⁢ cells,” Lamouille said.

The Lamouille lab focuses on how cancer cells communicate,particularly the role of connexin 43,a protein involved in cell-to-cell interaction.

Using super-resolution microscopy, Lamouille and James Smyth, associate professor,⁢ discovered that connexin 43 is strongly associated with microtubules in glioblastoma stem-like cells.

JM2, a connexin⁢ 43-derived peptide developed by Rob Gourdie, Heywood fralin professor at ‍the ‍Fralin Biomedical⁣ Research Institute, mimics the microtubule-interacting domain of connexin 43. It⁢ was then used to ⁤explore connexin 43’s role in glioblastoma stem cells.

“When we tested JM2 in⁤ glioblastoma stem-like cells, that was the most exciting moment,” Lamouille said. ⁣”Not only did that efficiently disrupt connexin 43 interaction with microtubules, but JM2 was also toxic specifically for these particular cells, ‍leaving healthy brain cells unharmed.”

The research indicates a novel⁤ tumorigenic function for connexin 43, extending beyond glioblastoma.

“I can remember ‍presentations ⁢by the ⁢team in which the three-dimensional⁤ gliospheres used to model tumors in the culture dish were clearly getting smaller,” said co-author Gourdie. “It⁢ was surprising to see such a drastic effect ‍on⁣ glioblastoma. The JM2 ‍peptide had a killing‍ effect by itself.⁤ That was unexpected.”

Further testing showed that JM2 disrupts the maintenance⁣ of treatment-resistant cancer cells and significantly ⁤slows ⁢tumor growth⁣ in animal models, supporting⁣ its ⁤potential as a new peptide-based drug for targeting glioblastoma stem cells.

Michael ⁤lunski, a carilion Clinic resident, and Zhi Sheng, assistant professor, also contributed to the research, using ⁤glioblastoma cells‍ derived from ‍tumor cells donated by brain cancer patients receiving care from Carilion⁤ physicians.

What’s next

Lamouille is now⁢ experimenting with delivery mechanisms to target the JM2 peptide ‍specifically to glioblastoma cells, including biodegradable nanoparticles and viral‍ vectors. Lamouille ⁢and Gourdie are co-founders of Acomhal Research Inc., which licensed the JM2 peptide to develop new therapies for ⁣cancer patients. While ⁤more research ⁣is‍ needed, preclinical findings suggest that combining JM2 with chemotherapy could improve patient survival by slowing recurrence.