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Enhancement of radiosensitivity in human esophageal carcinoma cells by fenofibrate and its potential mechanism

Abstract

Aims and Background

Fenofibrate is a specific agonist of PPARα, and is characterized by relatively low systemic toxicity. Recent studies have revealed that fenofibrate suppresses the growth of several cancer lines in vitro, but the exact relation between fenofibrate and irradiation has not been explored. The purpose of this study was to investigate the radiosensitivity enhancement effects of fenofibrate combined with radiation on the human esophageal carcinoma cell lines Eca-109 and TE1, and the potential mechanism underlying these effects.

Methods and Study design

The Eca-109 and TE1 cell lines were tested by the CCK-8 assay for cell proliferation. The multitarget click model was used to delineate the survival curve and radiosensitivity was determined after cells were treated with fenofibrate and/or x-ray radiation. Flow cytometry was used to examine the effect of fenofibrate and radiation on the cell cycle. The expression of vascular endothelial growth factor (VEGF) protein was detected by Western blot analysis.

Results

When given alone, fenofibrate had a time- and concentration-dependent cytotoxic effect on cells. The dose-enhancement ratio for combined fenofibrate and radiation increased markedly compared with fenofibrate alone. Further, the ratio of cells in the G2/M phase after fenofibrate and radiation was higher than that after fenofibrate or irradiation alone. The expression of VEGF protein was suppressed after treatment with fenofibrate alone or fenofibrate plus radiation.

Conclusions

Fenofibrate can enhance the radiosensitivity of human esophageal carcinoma cells by increasing G2/M phase arrest. Modulation of VEGF expression could contribute in vivo to a favorable interaction.

Tumori 2015; 101(1): 123 - 130

Article Type: ORIGINAL RESEARCH ARTICLE

DOI:10.5301/tj.5000228

Authors

Xiao-Qing Li, Jun-Dong Zhou, Shi-Tao Zou, Jian Yu, Xin-Jun Meng, Jin-Chang Wu

Article History

Disclosures

Financial support: This work was supported by the National Natural Science Foundation of China (81372433), the Nature Science Foundation of Jiangsu Province (BK20131149), and Suzhou Administration of Science & Technology (SYS201360 and SYS201254).
Conflict of interest: The authors have no conflict of interest.

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Authors

Affiliations

  • The Core Laboratory of Suzhou Cancer Center, Nanjing Medical University Affiliated Suzhou Hospital, Suzhou - China
  • Department of Radiotherapy, Nanjing Medical University Affiliated Suzhou Hospital, Suzhou - China
  • Xiao-Qing Li and Jun-Dong Zhou contributed equally to this work

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