Use of valproic acid in the preparation of a radiosensitizer for lung adenocarcinoma

By regulating the radiation sensitivity of lung adenocarcinoma cells with valproic acid and targeting the GLIPR2 protein to inhibit BECN1 activity, the problem of radiotherapy resistance in lung adenocarcinoma was solved, and the radiotherapy effect was significantly improved.

CN120204195BActive Publication Date: 2026-07-24NANTONG TUMOR HOSPITAL
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Patent Information

Application Number
CN202510462645.5
Authority / Receiving Office
CN · China
Patent Type
Patents(China)
Current Assignee / Owner
Filing Date
2025-04-14
Publication Date
2026-07-24
Estimated Expiration
2045-04-14

AI Technical Summary

Technical Problem

In the current technology, lung adenocarcinoma patients are resistant to radiotherapy, resulting in a low 5-year survival rate, and there is a lack of effective radiosensitizers.

Method used

Valproic acid (VPA) was used to regulate the radiation sensitivity of lung adenocarcinoma cells, and the activity of the autophagy marker BECN1 was inhibited by targeting the GLIPR2 protein, thereby enhancing the effect of radiotherapy.

Benefits of technology

At low concentrations, VPA significantly enhances the sensitivity of lung adenocarcinoma cells to radiotherapy, reduces colony formation, promotes radiosensitization, and improves the killing effect on lung adenocarcinoma cells.

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Abstract

The application discloses application of valproic acid in preparation of a lung adenocarcinoma radiotherapy sensitizer and belongs to the technical field of biological medicine. The application discloses application of valproic acid in preparation of a lung adenocarcinoma radiotherapy sensitizer, and low-concentration valproic acid significantly enhances the sensitivity of lung adenocarcinoma cells PC9 and H1299 to radiation; at a concentration far lower than the half-inhibitory concentration of VPA, 5 muM VPA significantly enhances the sensitivity of lung adenocarcinoma cells PC9 and H1299 to radiotherapy. Valproic acid inhibits BECN1 by promoting GLIPR2 expression, VPA combined with irradiation significantly promotes the combination of GLIPR2 and BECN1, thereby inhibiting the activity of the autophagy marker BECN1 and reducing the occurrence of autophagy; VPA improves the sensitivity of lung adenocarcinoma cells to radiotherapy by targeting GLIPR2.
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