Open Access
ARTICLE
Overexpression of Forkhead Box L1 (FOXL1) Inhibits the Proliferation and Invasion of Breast Cancer Cells
* Department of Pathology, Xinxiang Medical University, Xinxiang, P.R. China
† Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine in Henan Province,
School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, P.R. China
‡ Department of Pathology, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, P.R. China
§ Research Center for Immunology, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, P.R. China
Oncology Research 2017, 25(6), 959-965. https://doi.org/10.3727/096504016X14803482769179
Abstract
Forkhead box L1 (FOXL1) is a member of the Forkhead box (FOX) superfamily and was reported to be dysregulated in various types of cancers. However, its expression pattern and underlying cellular function in breast cancer remain largely unexplored. Thus, the aim of this study was to detect FOXL1 expression in breast cancer and to analyze its role in the progression of breast cancer. Our results demonstrated that FOXL1 expression at both the mRNA and protein levels was downregulated in breast cancer tissues and cell lines. Ectopic FOXL1 suppressed breast cancer cell proliferation, migration, and invasion in vitro. Furthermore, overexpression of FOXL1 significantly attenuated tumor growth in breast xenograft models in vivo. Finally, overexpression of FOXL1 significantly downregulated the protein expression levels of β-catenin, c-Myc, and cyclin D1 in MDAMB-231 cells. Taken together, the present study demonstrated that FOXL1 inhibited the proliferation, invasion, and migration of breast cancer in vitro and breast tumor growth in vivo through deactivating the Wnt/β-catenin signaling pathway. Thus, these findings suggest that FOXL1 may be a potential novel target for breast cancer therapy.Keywords
Cite This Article
This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.