Etoposide radiosensitizes p53-defective cholangiocarcinoma cell lines independent of their G2 checkpoint efficacies

Hematulin,Arunee; Meethang,Sutiwan; Utapom,Kitsana; Wongkham,Sopit; Sagan,Daniel

doi:10.3892/ol.2018.7754

Etoposide radiosensitizes p53-defective cholangiocarcinoma cell lines independent of their G2 checkpoint efficacies

Authors:
- Arunee Hematulin
- Sutiwan Meethang
- Kitsana Utapom
- Sopit Wongkham
- Daniel Sagan
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Affiliations: Radiobiology Research Laboratory, Department of Radiation Technology, Faculty of Allied Health Sciences, Naresuan University, Phitsanulok 65000, Thailand, Radiation Oncology Unit, Department of Radiology, Faculty of Medicine, Naresuan University, Phitsanulok 65000, Thailand, Department of Biochemistry, Liver Fluke and Cholangiocarcinoma Research Center, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand, Independent Researcher, Miesbach, D‑83714 Bavaria, Germany
Published online on: January 9, 2018 https://doi.org/10.3892/ol.2018.7754
Pages: 3895-3903

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Abstract

Radiotherapy has been accounted as the most comprehensive cancer treatment modality over the past few decades. However, failure of this treatment modality occurs in several malignancies due to the resistance of cancer cells to radiation. It was previously reported by the present authors that defective cell cycle checkpoints could be used as biomarkers for predicting the responsiveness to radiation in individual patients with cholangiocarcinoma (CCA). However, identification of functional defective cell cycle checkpoints from cells from a patient's tissues is cumbersome and not applicable in the clinic. The present study evaluated the radiosensitization potential of etoposide in p53‑defective CCA KKU‑M055 and KKU‑M214 cell lines. Treatment with etoposide enhanced the responsiveness of two p53‑defective CCA cell lines to radiation independent of G2 checkpoint function. In addition, etoposide treatment increased radiation‑induced cell death without altering the dominant mode of cell death of the two cell lines. These findings indicate that etoposide could be used as a radiation sensitizer for p53‑defective tumors, independent of the function of G2 checkpoint.

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