Objective:To evaluate the effect of Salvianolic acid B on the radiosensitivity of human non-small cell lung cancer cells and investigate its possible mechanism.Methods:Non-small cell lung cancer cells A549 and H1299 were cultured in vitro. The toxicity of Salvianolic acid B on non-small cell lung cancer cells was detected by MTT assay. The effect of Salvianolic acid B on the radiosensitivity was assessed by clone formation assay. Transwell chamber assay was used to evaluate the effect of Salvianolic acid B on the migration of tumor cells. Western blot was employed to detect the expression levels of OTUD7B, MMP-2, MMP-9, E-cadherin, Akt and p-Akt regulated by Salvianolic acid B. Results:Salvianolic acid B (5 μmol/L) could inhibit the proliferation of A549 and H1299 cells. Clone formation assay showed that Salvianolic acid B increased the radiosensitivity of A549 and H1299 cells, with a radiosensitization ratio of 1.45 and 1.38, respectively. Transwell chamber assay indicated that the ability of cell migration was significantly inhibited by Salvianolic acid B ( P<0.05). Western blot revealed that the expression levels of OTUD7B in A549 and H1299 cells were induced by irradiation in a time-dependent manner. Salvianolic acid B could down-regulate the expression levels of MMP-2, MMP-9 and p-Akt, whereas up-regulate the expression level of E-cadherin by down-regulating the expression level of OTUD7B. Conclusions:Salvianolic acid B can enhance the radiosensitivity of A549 and H1299 cells. The possible mechanism is that Salvianolic acid B down-regulates the expression level of OTUD7B induced by irradiation and inhibits the epithelial-mesenchymal transition process of tumor cells.

Objective:To investigate the effect of salvia miltiorrhiza-derived Sal-miR-58 on the radiosensitivity of glioma U251 cells and its possible mechanism. Methods:Glioma U251 cells were treated with different concentrations of miR-Ctl or Sal-miR-58 mimic, and subsequently treated with radiation to establish the radiotherapy model in vitro. The effect of Sal-miR-58 upon U251 cell viability was assessed by MTT assay. The effect of Sal-miR-58 on apoptosis of glioma U251 cells was evaluated by Hoechst33342/ propidium iodide (PI) staining. The changes of reactive oxygen species (ROS) content in U251 cells were detected by 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA) fluorescent probe. The effect of Sal-miR-58 combined irradiation on the radiosensitivity of U251 cells was detected by clone formation assay. The expression levels of HCLS1-related protein X-1 (HAX1), apoptosis marker proteins B cell lymphoma 2 (Bcl-2), cleaved-cysteine-containing aspartate-specific protease (Cleaved-Caspase) 9 and Cleaved-Caspase 3 were detected by Western blot. Multi-group comparison was conducted by one-way ANOVA. Two-group comparison was performed by independent sample t-test. Results:Sal-miR-58 could exacerbate the inhibition of U251 cell proliferation after irradiation ( P<0.05). Sal-miR-58 could promote the apoptosis of U251 cells and increase the production of ROS in U251 cells after radiation ( P<0.05). Clone formation assay showed that Sal-miR-58 increased the radiosensitivity of U251 cells, with a radiosensitization ratio of 1.43. Western blot showed that Sal-miR-58 inhibited the expression of HAX1 in U251 cells. Sal-miR-58 could inhibit the expression of Bcl-2 and increase the activation of Caspase 3 and Caspase 9 by reducing the expression of HAX1. Conclusions:Sal-miR-58 enhances the radiosensitivity of U251 cells. The possible mechanism is that Sal-miR-58 inhibits the expression of HAX1 induced by radiation and accelerates the apoptosis process of tumor cells.