NDLI: Inhibition of cyclin D1 enhances sensitivity to radiotherapy and reverses epithelial to mesenchymal transition for esophageal cancer cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Su, Huafang Jin, Xiance Shen, Lanxiao Fang, Ya Fei, Zhenghua Zhang, Xuebang Xie, Congying Chen, Xiaolei
Description	Country affiliation: China Author Affiliation: Su H ( Department of Radiotherapy and Chemotherapy, The First Affiliated Hospital of Wenzhou Medical University, No. 2 Fuxue Lane, Wenzhou, 325000, China.); Jin X ( Department of Radiotherapy and Chemotherapy, The First Affiliated Hospital of Wenzhou Medical University, No. 2 Fuxue Lane, Wenzhou, 325000, China.); Shen L ( Department of Radiotherapy and Chemotherapy, The First Affiliated Hospital of Wenzhou Medical University, No. 2 Fuxue Lane, Wenzhou, 325000, China.); Fang Y ( Department of Radiotherapy and Chemotherapy, The First Affiliated Hospital of Wenzhou Medical University, No. 2 Fuxue Lane, Wenzhou, 325000, China.); Fei Z ( Department of Radiotherapy and Chemotherapy, The First Affiliated Hospital of Wenzhou Medical University, No. 2 Fuxue Lane, Wenzhou, 325000, China.); Zhang X ( Department of Radiotherapy and Chemotherapy, The First Affiliated Hospital of Wenzhou Medical University, No. 2 Fuxue Lane, Wenzhou, 325000, China.); Xie C ( Department of Radiotherapy and Chemotherapy, The First Affiliated Hospital of Wenzhou Medical University, No. 2 Fuxue Lane, Wenzhou, 325000, China. wzxiecongying@163.com.); Chen X ( Department of Gastrointestinal Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China. billy07@wzhospital.cn.)
Abstract	Acquired radioresistance during radiotherapy has significantly affected the treatment efficacy in esophageal cancer. Many of radioresistant cancer cells demonstrated epithelial-mesenchymal transition (EMT).We found in previous study that a radioresistant cell line (KYSE-150R) possessed EMT characteristic with cyclin D1 overexpression. Cyclin D1 has been demonstrated to affect the radiation sensitivity in cancer cells. To elucidate the molecular functions of cyclin D1 on EMT phenotypes and esophageal cancer radiosensitivity, we treated the radioresistant esophageal cancer cells (KYSE-150R) and parental cells (KYSE-150) with cyclin D1 small interfering RNA (siRNA). The cell proliferation rate of KYSE-150R and the radiation survival fraction were significantly decreased in cyclin D1 siRNA treatment group. Knocking down cyclin D1 resulted in G0/G1 arrest in KYSE-150R cells. The average number of irradiation-induced Î³-H2AX foci increased in the cells treated with cyclin D1 siRNA, indicating impaired DNA double-strand break (DSB) repair in KYSE-150R cells. Cyclin D1 also reversed EMT phenotypes with significantly increased expression of E-cadherin in KYSE-150R cells. However, cyclin D1 siRNA have no radiosensitizing effects on KYSE-150 cells, with no obvious change in EMT marker expression .Our work showed that EMT phenotypes can be reduced and the radiosensitivity of esophageal cancer cells can be enhanced by inhibiting cyclin D1.
File Format	HTM / HTML
ISSN	10104283
Issue Number	4
Journal	Tumor Biology
Volume Number	37
e-ISSN	14230380
Language	English
Publisher	Springer
Publisher Date	2016-04-01
Publisher Place	Netherlands
Access Restriction	Subscribed
Content Type	Text
Resource Type	Article
Subject	Medicine Cancer Research

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