机构：[1]Department of Thyroid and Breast Surgery, The Third People’s Hospital of Shenzhen, Shenzhen, Guangdong518112, China深圳市康宁医院深圳医学信息中心[2]Department ofBreast Surgery, Maternal and Child Health Care Hospital of Hunan Province, Changsha, Hunan 410008,China[3]School of Clinical Medicine,Xiangnan University, Chenzhou,Hunan 423000, China[4]Department of Medical Examination, Zhuzhou Central Hospital, Zhuzhou, Hunan412007, China[5]Department of General Surgery, The Third Hospitalof Changsha, Changsha, Hunan410013, China[6]Department of Gastrointestinal and Breast and Thyroid Surgery, Changsha Hospitalof Traditional Chinese Medicine (Changsha Eighth Hospital), Changsha,Hunan 410100, China[7]Departmentof Surgery, The Medical School,University of South China, Hengyang,Hunan 421000, China
Breast cancer is the most common cancer among women with ~1.67 million cases diagnosed annually worldwide, and ~1 in 37 women succumbed to breast cancer. Over the past decades, new therapeutic strategy has substantially improved the curative effect for women with breast cancer. However, the currently available ER-targeted and HER-2-based therapies are not effective for triple-negative breast cancer patients, which account for ~15% of total breast cancer cases.
We reported that 1,25-(OH)2D3, a biologically active form of vitamin D3, exhibited a strong anticancer effects on the proliferation, migration, invasion, cell cycle arrest, and apoptosis of both ER-positive (MCF-7) and ER-negative breast cancer cells (MDA-MB-453).
The anticancer effect of 1,25-(OH)2D3 was more potent compared to the classical chemotherapeutics tamoxifen in MDA-MB-453 cells. Furthermore, we also found that 1,25-(OH)2D3 decreased the expression of Ras and resulted in decrease of the phosphorylation of downstream proteins MEK and ERK1/2, indicating that 1,25-(OH)2D3 plays its anticancer roles through targeting the Ras/MEK/ERK signaling pathway. In addition, Ras overexpression abrogated 1,25-(OH)2D3-induced G0/G1 cell cycle arrest and apoptosis of breast cancer cells, as well as the suppression of proliferation, migration, and invasion. Our study suggested that 1,25-(OH)2D3 suppressed breast cancer tumorigenesis by targeting the Ras/MEK/ERK signaling pathway.
1,25-(OH)2D3 might serve as a promising supplement for breast cancer drug therapy, especially for the ER-negative breast cancer and drug-resistant breast cancer.
基金：
This research is supported by the Project of Science and Technology Department of Hunan Province (2013SK3189), Scientific Research Fund of Hunan Provincial Education Department (No 15B225), and Scientific Research Fund of Hunan Provincial Health and Family Planning Commission (No C2017014).
第一作者机构：[1]Department of Thyroid and Breast Surgery, The Third People’s Hospital of Shenzhen, Shenzhen, Guangdong518112, China[*1]Department of Thyroid and Breast Surgery, The Third People’s Hospital of Shenzhen, 29 Bulan Road, Longgang District, Shenzhen, Guangdong 518112, China
通讯作者：
通讯机构：[1]Department of Thyroid and Breast Surgery, The Third People’s Hospital of Shenzhen, Shenzhen, Guangdong518112, China[*1]Department of Thyroid and Breast Surgery, The Third People’s Hospital of Shenzhen, 29 Bulan Road, Longgang District, Shenzhen, Guangdong 518112, China
推荐引用方式(GB/T 7714)：
Zheng Wei,Cao Lin,Ouyang Linna,et al.Anticancer activity of 1,25-(OH)2D3 against human breast cancer cell lines by targeting Ras/MEK/ERK pathway.[J].ONCOTARGETS AND THERAPY.2019,12:721-732.doi:10.2147/OTT.S190432.
APA：
Zheng Wei,Cao Lin,Ouyang Linna,Zhang Qian,Duan Bofeng...&Gong Daoxing.(2019).Anticancer activity of 1,25-(OH)2D3 against human breast cancer cell lines by targeting Ras/MEK/ERK pathway..ONCOTARGETS AND THERAPY,12,
MLA：
Zheng Wei,et al."Anticancer activity of 1,25-(OH)2D3 against human breast cancer cell lines by targeting Ras/MEK/ERK pathway.".ONCOTARGETS AND THERAPY 12.(2019):721-732
