Oncotarget

Reviews:

Pathogenic roles of alterations in vitamin D and vitamin D receptor in gastric tumorigenesis

Chao Du, Shiming Yang, Xiaoyan Zhao _ and Hui Dong

PDF  |  HTML  |  How to cite

Oncotarget. 2017; 8:29474-29486. https://doi.org/10.18632/oncotarget.15298

Metrics: PDF 2258 views  |   HTML 3078 views  |   ?  


Abstract

Chao Du1,2, Shiming Yang1, Xiaoyan Zhao1 and Hui Dong1,3

1 Department of Gastroenterology, Xinqiao Hospital, Third Military Medical University, Chongqing, China

2 Department of Gastroenterology and Hepatology, Chengdu Military General Hospital, Chengdu, Sichuan Province, China

3 Division of Gastroenterology, Department of Medicine, School of Medicine, University of California, San Diego, California, USA

Correspondence to:

Xiaoyan Zhao, email:

Hui Dong, email:

Keywords: vitamin D, vitamin D receptor, gastric cancer, tumorigenesis

Received: December 10, 2016 Accepted: January 20, 2017 Published: February 11, 2017

Abstract

Gastric cancer is currently the second leading cause of cancer-related death worldwide, especially in Japan, Korea and China, and the 5-year survival rate of gastric cancer is less than 30%. Thus, it is important to shed more lights on novel agents to prevent gastric cancer or to improve survival rate of the patients. Vitamin D not only maintains calcium and bone homeostasis, but also mostly inhibits tumor genesis, invasion, and metastasis through activation of vitamin D receptor. Although epidemiological results are not consistent, accumulating evidence from gastric cancer cells, animal models, and clinical trials suggest that vitamin D deficiency may increase the risk and mortality of gastric cancer, but vitamin D supplement might be a safe and economical way to prevent or treat gastric cancer. Here, we reviewed the current studies on vitamin D and its receptor and focused on the pathogenic roles of their alterations in gastric tumorigenesis.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 15298