ArticleRNA biology2026
Bevacizumab induces apoptosis in glioblastoma cells by upregulating miR-4695-5p to inhibit PKMYT1.
Article in RNA biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
We sought to determine the pro-apoptotic effects of bevacizumab in glioblastoma (GBM) and to elucidate the contribution of the miR-4695-5p/PKMYT1 pathway to this process. Following treatment of U87MG and U251 GBM cells with dose-gradient bevacizumab, cellular responses were evaluated by measuring apoptosis (flow cytometry) and proliferation (CCK-8), while RT-qPCR quantified changes in miR-4695-5p, Bax, and Bcl-2 expression. PKMYT1, bioinformatically predicted as a downstream target of miR-4695-5p, was verified via luciferase reporter assays. The functional link between miR-4695-5p and PKMYT1 was established using miRNA mimics and PKMYT1 overexpression rescue experiments. The critical role of this pathway in bevacizumab-induced apoptosis was ultimately confirmed by co-treating cells with bevacizumab and either a miR-4695-5p inhibitor or a PKMYT1 overexpression vector. Bevacizumab induced apoptosis in GBM cells U87MG and U251 in a dose-dependent manner. After bevacizumab treatment, the expression level of miR-4695-5p increased, and inhibiting miR-4695-5p expression reduced the pro-apoptotic effect of bevacizumab on U87MG and U251 cells. miR-4695-5p could target and inhibit PKMYT1 expression. Overexpression of PKMYT1 suppressed the pro-apoptotic effect of bevacizumab on U87MG and U251 cells, indicating that bevacizumab induces apoptosis in GBM cells by upregulating miR-4695-5p to target and inhibit PKMYT1. This study reveals the role and mechanism of bevacizumab in inducing apoptosis in GBM cells, namely by upregulating miR-4695-5p expression to target and inhibit the expression of the anti-apoptotic protein PKMYT1, thereby inducing apoptosis in GBM cells. This provides new directions and targets for research and treatment of gliomas.
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