The Aptamer bi-(AID-1-T) Synergizes with Radiation to Inhibit Proliferation of Human Glioma Cells
<b>Background:</b> High-grade gliomas are treatment-resistant and prone to aggressive recurrence. Although radiation therapy is a fundamental treatment, it often fails to eradicate tumors and can enhance the migratory potential of surviving cells, promoting relapse. Anti-proliferative aptamers are novel agents that show promise, but their combination with radiation therapy and their effects on invasive phenotypes require further investigation. <b>Objectives:</b> This study evaluated the effects of ionizing radiation on the viability and migration of human glioma cells, both alone and in combination with the anti-proliferative aptamer bi-(AID-1-T). The study aimed to determine whether the aptamer could enhance the efficacy of radiotherapy and counteract ionizing radiation-induced pro-migratory effects. <b>Methods:</b> The study was conducted on cell cultures of primary and relapsed human glioma. The effects of combined radiation (single dose of 20 Gy) and the bi-(AID-1-T) aptamer (10 μM) were assessed using the MTS assay, Transwell analysis, immunocytochemistry and transcriptome analysis. <b>Results:</b> Ionizing radiation alone reduced proliferation in primary gliomas, but increased proliferation in recurrent cultures. Ionizing radiation also increased migration in both types of gliomas. Combining ionizing radiation with the bi-(AID-1-T) aptamer produced a synergistic effect: it significantly reduced cell proliferation and migration, and suppressed the ionizing radiation-induced migratory enhancement, more effectively than either treatment alone. Transcriptome analysis revealed that combination treatment decreased the expression of pro-proliferative and migratory genes (e.g., <i>PDPN</i>, <i>CDH3</i>), while increasing the expression of anti-migratory (<i>RND3</i>) and pro-apoptotic genes (e.g., <i>XAF1</i>, <i>SEMA3A</i>). Thus, combination treatment significantly reduces tumor cell proliferation and migration; however, further studies on surviving cells are needed.
Authors
- Mikhail Galkin (ORCID: https://orcid.org/0000-0002-1436-0010)
- A. V. Ryabova (ORCID: https://orcid.org/0000-0003-3488-1128)
- Svetlana Pavlova (ORCID: https://orcid.org/0000-0002-9595-9358)
- Alexey Kopylov (ORCID: https://orcid.org/0000-0003-0962-8905)
- Andrey Golanov (ORCID: https://orcid.org/0000-0002-0976-4547)
- Galina Pavlova (ORCID: https://orcid.org/0000-0002-6885-6601)
- L. V. Fab
- A. V. Revishchin (ORCID: https://orcid.org/0000-0002-6007-6440)
- Ekaterina Savchenko
- Dmitrij Usachev (ORCID: https://orcid.org/0000-0003-1520-5650)
- Natalia Antipina (ORCID: https://orcid.org/0000-0003-3470-5802)
- Nadezhda Samoylenkova
- Ksenia Rubetskaya (ORCID: https://orcid.org/0009-0006-3845-558X)
Institutions
- Sechenov University (RU)
- Lomonosov Moscow State University (RU)
- Ministry of Health of the Russian Federation (RU)
- Burdenko Neurosurgery Institute (RU)
- Prokhorov General Physics Institute (RU)
- Institute of Higher Nervous Activity and Neurophysiology (RU)
Publication Details
- Journal
- Pharmaceutics
- Published
- 2025-11-08
- DOI
- https://doi.org/10.3390/pharmaceutics17111442
- Primary Topic
- Glioma Diagnosis and Treatment
- Type
- article
- Field-Weighted Citation Impact
- 0.00