Glioblastoma is one of the deadliest forms of brain cancer. Even with surgery, radiation, and chemotherapy, it almost always comes back.
Most patients survive just over 14 months after diagnosis, and current treatments cannot prevent the return of the tumor.
A new study from scientists at Virginia Tech’s Fralin Biomedical Research Institute at VTC suggests there may be a way to slow this recurrence.
The team has been studying a lab-designed molecule called JM2, which targets a hidden weakness in glioblastoma’s most dangerous cells — the ones that can survive treatment and regrow the tumor.
The research, published in Cell Death and Disease, focuses on glioblastoma stem cells. These are special cancer cells that resist chemotherapy and radiation. They can stay dormant for a while, then “wake up” and start building the tumor again.
According to lead researcher Samy Lamouille, these cells adapt easily to their surroundings and are very hard to destroy. “It’s critical to find a way to target this population of cancer cells,” he said.
Lamouille’s lab studies how cancer cells communicate with each other, focusing on a protein called connexin 43. This protein helps form gap junctions — tiny channels that allow cells to share signals directly. Connexin 43 has a complex role in cancer: in some situations, it can help block tumor growth, but in others, it can help cancer spread.
Using advanced imaging technology called super-resolution microscopy, Lamouille and colleague James Smyth found that in glioblastoma stem cells, connexin 43 attaches strongly to microtubules — tiny structural fibers inside cells — along their entire length. This was the first time scientists had seen this connection in these cancer cells.
Building on that discovery, the team tested JM2, a small peptide (a short chain of amino acids) designed to mimic part of connexin 43 that binds to microtubules. JM2 was originally developed by researcher Rob Gourdie while at the Medical University of South Carolina.
When JM2 was applied to glioblastoma stem cells in the lab, it disrupted the link between connexin 43 and microtubules. Even more exciting, it was toxic to these cancer stem cells but left healthy brain cells unharmed. Importantly, JM2 did this without interfering with connexin 43’s other important roles in the cell.
In lab tests, JM2 on its own shrank 3D tumor-like cell clusters. Further experiments in animal models showed that JM2 slowed tumor growth and reduced the population of treatment-resistant cancer cells. These results suggest JM2 could help delay glioblastoma’s return after standard treatments.
The study also benefited from a collaboration with Carilion Clinic, a health system in Southwest Virginia. Tumor cells used in the experiments were donated by local brain cancer patients, with their consent, after surgery. This partnership between research labs and clinical teams helped move the discovery forward.
Although JM2 is still in the early stages of development, the researchers believe it could eventually be combined with chemotherapy to improve survival. They are now working on targeted delivery methods, such as biodegradable nanoparticles and viral vectors, to ensure the drug reaches glioblastoma cells more effectively.
Lamouille and Gourdie have co-founded a company, Acomhal Research Inc., to help bring JM2 closer to clinical use. More research will be needed to confirm its safety and effectiveness in humans, but the early findings offer hope for tackling one of the most treatment-resistant cancers known.
This study is promising because it targets the root cause of glioblastoma recurrence — the stem cells that survive treatment and rebuild tumors. By disrupting a newly discovered connection between connexin 43 and microtubules, JM2 selectively kills these cells while sparing healthy brain tissue.
The fact that JM2 works both in cell cultures and in animal models makes it a strong candidate for future clinical testing. If delivery methods can be optimized and safety confirmed, JM2 could be an important addition to brain cancer treatment.
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