Research Papers:
Targeting stearoyl-CoA desaturase 1 to repress endometrial cancer progression
PDF | HTML | Supplementary Files | How to cite
Metrics: PDF 2096 views | HTML 2806 views | ?
Abstract
Weihua Li1,2, Huimin Bai2, Shiping Liu3, Dongyan Cao1, Hongying Wu4, Keng Shen1, Yanhong Tai5,* and Jiaxin Yang1,*
1Department of Obstetrics and Gynecology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Wangfujing, Beijing 100730, China
2Department of Obstetrics and Gynecology, Beijing Chao-Yang Hospital Affiliated to Capital Medical University, Beijing 100020, China
3Departments of Obstetrics and Gynecology, Peking University First Hospital, Beijing 100034, China
4Institute of Radiation Medicine, The Chinese Academy of Medical Sciences, Tianjin 300192, China
5Department of Pathology, The Affiliated Hospital of Military Medical Science Academy of Chinese People’s Liberation Army (307 Hospital of Chinese People’s Liberation Army), Beijing 100071, China
*These authors contributed equally to this work
Correspondence to:
Yanhong Tai, email: [email protected]
Jiaxin Yang, email: [email protected]
Keywords: stearoyl-CoA desaturase; endometrial cancer; therapeutic target; cell growth; cell death
Received: July 28, 2017 Accepted: December 26, 2017 Published: January 24, 2018
ABSTRACT
Stearoyl-CoA desaturase 1 (SCD1) is an established molecular target in many primary tumors including breast, lung, pancreatic, colon and hepatocellular carcinomas. However, its potential role in supporting endometrial cancer growth and progression has not yet been determined. In this study, we evaluated the value of SCD1 as a candidate therapeutic target in human endometrial cancer. Compared with secretory and post-menopausal endometrium, SCD1 was highly expressed in normal endometrium of proliferative phase, endometrial hyperplasia and endometrial carcinoma, while was absent or low expression in non-malignant control stromal cells and adjacent normal endometrium. Knockdown of SCD1 significantly repressed endometrial cancer cell growth and induced cell apoptosis. Both short hairpin RNA targeted knockdown and chemical inhibitor of SCD1 suppressed the foci formation of AN3CA, a metastatic endometrial cell line. Xenograft model further demonstrated that reduced SCD1 expression impaired endometrial cancer growth in vivo. Taken together, these findings indicate that SCD1 is a potentially therapeutic target in human endometrial cancer. Inhibiting lipid metabolism in cancer cells would be a promising strategy for anti-cancer therapy.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 24304