An antidepressant lowered two cancer-linked genes in brain tumor cells
Original title: Systemic Drug Effects in Vortioxetine-Induced Time-Series Datasets.
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 on cells in a lab dish, not in people.
The short version
This was a lab test on glioblastoma: The fastest-growing type of glioma (grade 4). Treatment usually starts soon after diagnosis: surgery first, then radiation and chemotherapy. See the glossary cells in a dish, not a treatment people can get.
What was studied. Researchers added vortioxetine, an antidepressant, to glioblastoma: The fastest-growing type of glioma (grade 4). Treatment usually starts soon after diagnosis: surgery first, then radiation and chemotherapy. See the glossary cells. They tracked how the cells' genes turned each other up or down at 0, 3, 6, 9, 12, and 24 hours.
What they found. Over time, the drug turned down JUN and CCND1. Both of these genes are linked to cancer growth. Two other genes tied to cancer growth, CDK4 and CCND1, were also turned down across all three sets of cells. Some genes went the other way and were turned up, including PIK3R5.
What this means, and what it doesn't
What it could mean: It gives scientists a reason to look further at this antidepressant and at these genes in glioblastoma: The fastest-growing type of glioma (grade 4). Treatment usually starts soon after diagnosis: surgery first, then radiation and chemotherapy. See the glossary. For a patient today, it changes nothing about care. No people were treated in this work.
What it doesn't mean: This does not mean vortioxetine treats brain tumors. It does not mean taking an antidepressant will shrink a tumor or help you live longer. This is lab stage work in cells in a dish. It has not been tested in people for this purpose. It is very far from everyday care, and it is not a cure or a promise of one.
Source: PubMed, July 6, 2026 · Read the original
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