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Cellular Redox Status Regulates Emodin-Induced Radiosensitization of Nasopharyngeal Carcinoma Cells In Vitro and In Vivo.

Hou H, Li D, Cheng D, Li L, Liu Y, Zhou Y - J Pharm (Cairo) (2013)

Bottom Line: HIF-1α expression significantly increased under hypoxic conditions but did not change after treatment with emodin alone.Compared to the CNE-1 xenografts exposed to radiation alone, CNE-1 xenografts exposed to radiation with emodin showed significantly enhanced radiation effects.Our data suggest that emodin effectively enhanced the radiosensitivity of CNE-1 cells in vitro and in vivo.

View Article: PubMed Central - PubMed

Affiliation: College of Pharmacy, Guangxi Medical University, Nanning 530021, China.

ABSTRACT
Here, we report that regulation of cellular redox status is required for radiosensitization of nasopharyngeal carcinoma (NPC) cells by emodin. We evaluated emodin's radiosensitivity-enhancing ability by using NPC cells in vitro and xenografts in vivo. A clonogenic assay was performed to evaluate NPC cell survival and to determine dose modification factors. Flow cytometry, western blot analysis, and in vivo radiation-induced tumor regrowth delay assays were performed to characterize emodin's effects. Exposure of CNE-1 NPC cells to emodin enhanced their radiosensitivity. HIF-1α expression significantly increased under hypoxic conditions but did not change after treatment with emodin alone. Emodin downregulated mRNA and protein expression of HIF-1α. Cells exposed to radiation and emodin underwent significant cell cycle arrest at the G2/M phase. The percentage of apoptotic cells and reactive oxygen species (ROS) levels were significantly higher in the group exposed to emodin and radiation hypoxic group than in the other groups. Compared to the CNE-1 xenografts exposed to radiation alone, CNE-1 xenografts exposed to radiation with emodin showed significantly enhanced radiation effects. Our data suggest that emodin effectively enhanced the radiosensitivity of CNE-1 cells in vitro and in vivo. The mechanism appears to involve ROS generation and ROS-mediated inhibition of HIF-1α expression.

No MeSH data available.


Related in: MedlinePlus

Fluorescence intensity of ROS in CNE-1 cell treated with radiation or combined with emodin.
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fig4: Fluorescence intensity of ROS in CNE-1 cell treated with radiation or combined with emodin.

Mentions: Following exposure of CNE-1 cells to noncytotoxic concentrations of emodin (3.9 μg/mL) or coadministration of emodin and radiation under hypoxic conditions for 24 h, the levels of ROS production were quantified using flow cytometry, monitoring fluorescence intensity. Compared to the control group, the relative content of ROS in CNE-1 cells determined at 24 h was 30.19 ± 2.69 in the hypoxic group, 117.71 ± 5.47 in the group exposed only to radiation, and 154.91 ± 6.25 in the group exposed to emodin combined with radiation (Table 5 and Figure 4). At 24 h, the relative amount of ROS in CNE-1 cells receiving emodin combined with radiation was significantly higher than those exposed to radiation alone, under hypoxic conditions (P < 0.05).


Cellular Redox Status Regulates Emodin-Induced Radiosensitization of Nasopharyngeal Carcinoma Cells In Vitro and In Vivo.

Hou H, Li D, Cheng D, Li L, Liu Y, Zhou Y - J Pharm (Cairo) (2013)

Fluorescence intensity of ROS in CNE-1 cell treated with radiation or combined with emodin.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4590808&req=5

fig4: Fluorescence intensity of ROS in CNE-1 cell treated with radiation or combined with emodin.
Mentions: Following exposure of CNE-1 cells to noncytotoxic concentrations of emodin (3.9 μg/mL) or coadministration of emodin and radiation under hypoxic conditions for 24 h, the levels of ROS production were quantified using flow cytometry, monitoring fluorescence intensity. Compared to the control group, the relative content of ROS in CNE-1 cells determined at 24 h was 30.19 ± 2.69 in the hypoxic group, 117.71 ± 5.47 in the group exposed only to radiation, and 154.91 ± 6.25 in the group exposed to emodin combined with radiation (Table 5 and Figure 4). At 24 h, the relative amount of ROS in CNE-1 cells receiving emodin combined with radiation was significantly higher than those exposed to radiation alone, under hypoxic conditions (P < 0.05).

Bottom Line: HIF-1α expression significantly increased under hypoxic conditions but did not change after treatment with emodin alone.Compared to the CNE-1 xenografts exposed to radiation alone, CNE-1 xenografts exposed to radiation with emodin showed significantly enhanced radiation effects.Our data suggest that emodin effectively enhanced the radiosensitivity of CNE-1 cells in vitro and in vivo.

View Article: PubMed Central - PubMed

Affiliation: College of Pharmacy, Guangxi Medical University, Nanning 530021, China.

ABSTRACT
Here, we report that regulation of cellular redox status is required for radiosensitization of nasopharyngeal carcinoma (NPC) cells by emodin. We evaluated emodin's radiosensitivity-enhancing ability by using NPC cells in vitro and xenografts in vivo. A clonogenic assay was performed to evaluate NPC cell survival and to determine dose modification factors. Flow cytometry, western blot analysis, and in vivo radiation-induced tumor regrowth delay assays were performed to characterize emodin's effects. Exposure of CNE-1 NPC cells to emodin enhanced their radiosensitivity. HIF-1α expression significantly increased under hypoxic conditions but did not change after treatment with emodin alone. Emodin downregulated mRNA and protein expression of HIF-1α. Cells exposed to radiation and emodin underwent significant cell cycle arrest at the G2/M phase. The percentage of apoptotic cells and reactive oxygen species (ROS) levels were significantly higher in the group exposed to emodin and radiation hypoxic group than in the other groups. Compared to the CNE-1 xenografts exposed to radiation alone, CNE-1 xenografts exposed to radiation with emodin showed significantly enhanced radiation effects. Our data suggest that emodin effectively enhanced the radiosensitivity of CNE-1 cells in vitro and in vivo. The mechanism appears to involve ROS generation and ROS-mediated inhibition of HIF-1α expression.

No MeSH data available.


Related in: MedlinePlus