Functional characterization of a novel transcript of ERCC1 in chemotherapy resistance of ovarian cancer
Metrics: PDF 980 views | HTML 2141 views | ?
Jia Liu1,*, Lin Zhang2,*, Ping Mao3,*, Guoqiang Jiang1, Likun Liu1, Jing Wang1, Wei Yang4, Lawrence Owusu1,5 and Weiling Li1
1Department of Biotechnology, Dalian Medical University, Dalian, Liaoning, 116044, China
2Academy of Integrative Medicine, Dalian Medical University, Dalian, Liaoning, 116044, China
3Department of General Surgery, The People’s Hospital of Liaoning Province, Shenyang, Liaoning, 110016, China
4Department of Pharmacy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Sheng 450000, China
5Department of Pharmaceutical Sciences, College of Pharmacy, University of South Florida, Tampa, FL 33612, USA
*These authors have contributed equally to this work
Weiling Li, email: email@example.com
Keywords: larger ERCC1 transcript, cisplatin resistance, ovarian cancer, MAPK pathway
Received: April 23, 2017 Accepted: July 25, 2017 Published: August 24, 2017
Approximately 15-20% of ovarian cancer patients receiving platinum-based chemotherapy are primary platinum-resistant. Identification of these patients and transfer to other more effective therapy could reduce the morbidity of ovarian cancer. ERCC1 is a DNA repair gene which can complex with XPF to repair cisplatin-induced DNA damage and cause chemotherapy resistance. In this study, we found a novel ERCC1 transcript initiated upstream of the normal transcription initiation site. The expression of this larger ERCC1 transcript dramatically increased following cisplatin treatment in ovarian cancer cells and was regulated by the MAPK pathway. This phenomenon conferred enhanced cisplatin resistance on ovarian cancer cells, and was confirmed with chemosensitive and chemoresistant patients’ samples. Our data suggested that larger ERCC1 transcript levels correlated with the outcome of platinum-based chemotherapy.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.