Lab study points to a new way to block a protein that drives some ependymomas
Original title: Distinct nuclear localization signals confer differential microtubule dependence among ZFTA fusion oncoproteins.
How far along is this research?
- Lab cells
- Animals
- Review
- Tested in people
This was done on cells in a lab, not in people. It is a very early step.
This was only done in lab cells, not in people.
The short version
In lab tests, an old drug called colchicine kept a tumor-driving protein from reaching the control center of the cell.
What was studied. Ependymoma is a type of brain and spine tumor. Some of these tumors are driven by a joined-together protein called ZFTA-RELA. Researchers screened 9600 different chemical compounds in the lab to find one that could shut down the genes this protein turns on.
What they found. The screen pointed to colchicine, a drug that breaks down tiny cell fibers called microtubules. Colchicine turned down genes that the ZFTA-RELA protein had switched on. It also partly kept that protein out of the cell nucleus, where it does its damage. Colchicine had the same effect on two related fusion proteins, ZFTA-NCOA2 and ZFTA-MKL2, but not on ZFTA-MAML2 or ZFTA-MAML3.
What this means, and what it doesn't
What it could mean: This kind of ependymoma resists chemotherapy and is hard to treat. The study suggests that the way these proteins travel into the nucleus could be a target for future drugs. It also suggests that different versions of the fusion protein may need different approaches.
What it doesn't mean: This work was done in the lab, not in people. No patient was treated in this study. It does not show that colchicine helps anyone with a brain tumor, and colchicine is not a treatment for ependymoma. This is early science, many years and many steps away from everyday care. It is not a cure or a promise of one.
Source: PubMed, July 13, 2026 · Read the original
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