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Galangin (GLN) Promotes Temozolomide-Induced Apoptosis in Glioma Cells

  • CELL BIOLOGY
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Abstract

The efficacy of Temozolomide (TMZ)-based chemotherapy in human malignancy is limited by the occurrence of innate and acquired drug resistance. Hence, in the present study, we tend to evaluate the effects of Galangin (GLN) combined with TMZ on proliferation and migration and its underlying mechanisms in the U251 cells of glioblastoma. MTT assay and cell death ELISA kit evaluated cellular proliferation and apoptosis, respectively. The mRNA levels of invasive genes were evaluated using the qRT-PCR. We also applied DCFH-DA fluorescence dye to detect reactive oxygen species (ROS) formation and activities of antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase, and glutathione S-transferase) in U251 cells. GLN considerably increased the cytotoxic effects of TMZ on the proliferation of U251 cells (P < 0.01). Also, this co-treatment potentiated the apoptosis rate in these tumor cells (P < 0.001). This outcome is achieved by decreasing metastatic and invasive genes (VEGF-A, MMP2, MMP9, and EpCAM). Moreover, ROS levels were increased (P < 0.01), and antioxidant enzymes’ expression levels were significantly decreased in the co-treatment group compared to the alone treatment with GLN or TMZ in U251 cells. Findings demonstrate a novel mechanism by which GLN enhances the cytotoxic effects of TMZ on tumor cells. This combinational therapy might promise a therapeutic regimen for improving the clinical efficacy in glioma patients.

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Correspondence to Yiyun Li.

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The authors declare that they have no conflicts of interest. This article does not contain any studies involving animals or human participants performed by any of the authors.

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Yiyun Li, Wan, Y., Yu, N. et al. Galangin (GLN) Promotes Temozolomide-Induced Apoptosis in Glioma Cells. Biol Bull Russ Acad Sci 49, 580–587 (2022). https://doi.org/10.1134/S1062359022060085

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