J Cancer 2018; 9(6):1078-1087. doi:10.7150/jca.23596 This issue

Research Paper

SULT1E1 inhibits cell proliferation and invasion by activating PPARγ in breast cancer

Yali Xu1, Xiaoyan Lin1, Jiawen Xu1, Haiyan Jing1, Yejun Qin1✉, Yintao Li2✉

1. Department of Pathology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong, P.R. China
2. Department of Medical Oncology, Shandong Cancer Hospital and Institute, Jinan, Shandong, P.R. China

This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) license (https://creativecommons.org/licenses/by-nc/4.0/). See http://ivyspring.com/terms for full terms and conditions.
Xu Y, Lin X, Xu J, Jing H, Qin Y, Li Y. SULT1E1 inhibits cell proliferation and invasion by activating PPARγ in breast cancer. J Cancer 2018; 9(6):1078-1087. doi:10.7150/jca.23596. Available from https://www.jcancer.org/v09p1078.htm

File import instruction


Sulfotransferase family 1E member 1 (SULT1E1) is known to catalyze sulfoconjugation and play a crucial role in the deactivation of estrogen homeostasis, which is involved in tumorigenesis and the progression of breast and endometrial cancers. Our previous study has shown that the protein levels of SULT1E1 were decreased in breast cancer; however, the underlying mechanism is still poorly understood. In this study, we explored the functional and molecular mechanisms by which SULT1E1 influenced breast cancer. Here, we identified that overexpression of SULT1E1 inhibited breast cancer cell growth through inducing apoptosis and arresting cell cycle progression. Furthermore, enforced expression of SULT1E1 suppressed tumor cell migration and invasion. Moreover, we found that the activation of PPARγ was required for SULT1E1-mediated downregulation of C-myc, Cyclin D1, MMP-2 and MMP-9 as well as for cell apoptosis, migration and invasion. In addition, the overexpression of SULT1E1 significantly inhibited tumor growth in vivo. Taken together, our findings indicated that SULT1E1 performed its tumor suppressor characteristics by activating PPARγ, which provided a novel target for patients with breast cancer.

Keywords: breast cancer, SULT1E1, PPARγ, proliferation, invasion