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Scutellarin improves the radiosensitivity of non‐small cell lung cancer cells to iodine‐125 seeds via downregulating the AKT/mTOR pathway

BACKGROUND: In our previous study, we indicated that scutellarin (SCU) induced an anticancer effect in A549 cells. However, whether SCU regulates the radiosensitivity of non‐small cell lung cancer (NSCLC) and its related mechanism is still unclear. METHODS: In this study, we explored the anticancer...

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Detalles Bibliográficos
Autores principales: He, Guang‐hui, Xing, Dian‐jin, Jin, Die, Lu, Yue, Guo, Lei, Li, Yu‐liang, Li, Dong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley & Sons Australia, Ltd 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8410549/
https://www.ncbi.nlm.nih.gov/pubmed/34255431
http://dx.doi.org/10.1111/1759-7714.14077
Descripción
Sumario:BACKGROUND: In our previous study, we indicated that scutellarin (SCU) induced an anticancer effect in A549 cells. However, whether SCU regulates the radiosensitivity of non‐small cell lung cancer (NSCLC) and its related mechanism is still unclear. METHODS: In this study, we explored the anticancer effect induced by iodine‐125 ((125)I) and SCU at a sensitizing concentration in A549 and H1975 cells. Cellular apoptosis and proliferation were detected by flow cytometry, Bcl‐2/Bax expression level, cell cycle, CCK‐8, and EdU staining. A tumor model using nude mice was also carried out to investigate the combined effect of (125)I and SCU in vivo. In addition, the expression level of AKT/mTOR pathway was detected to investigate whether it is linked to the anticancer effect of (125)I and SCU. RESULTS: SCU at a sensitizing concentration promoted the (125)I‐induced apoptosis and antiproliferative effect in A549 and H1975 cells. Moreover, the same results were obtained in vivo. Based on our findings, the AKT/mTOR pathway was significantly downregulated after combined treatment with (125)I and SCU. CONCLUSIONS: The results of our study suggested that SCU promotes the anticancer effects induced by (125)I in NSCLC cells by downregulating the AKT/mTOR pathway and lays a foundation for future application of this combined treatment.