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Overexpression of forkhead box J2 can decrease the migration of breast cancer cells
Author(s) -
Wang Yingying,
Yang Shuyun,
Ni Qichao,
He Song,
Zhao Yunhong,
Yuan Qin,
Li Chunmiao,
Chen Hongwei,
Zhang Li,
Zou Lin,
Shen Aiguo,
Cheng Chun
Publication year - 2012
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.24146
Subject(s) - vimentin , motility , breast cancer , metastasis , cancer research , western blot , immunofluorescence , biology , transcription factor , immunohistochemistry , cancer , antibody , immunology , microbiology and biotechnology , gene , biochemistry , genetics
Abstract The prognosis of breast cancer patients with metastases is generally poor, so it is essential to elucidate related molecules mechanisms. Forkhead Box J2 (FOXJ2) is a member of Forkhead Box transcription factors, many of which have been reported to participate in tumor migration and invasion. In this study, we showed the expression of FOXJ2 was higher in primary breast cancer tissues without lymph nodes metastases than those with, and there was statistical significance between the expression of FXOJ2 and the clinical factors. Hence, we identified a novel function of metastasis, which was not previously known for FOXJ2. Overexpression of FOXJ2 decreased the motility property of highly migrative MDA‐MB‐231 cells in vitro by wound healing assays and trans‐well migration assays, and it was concurrent with the increased expression of epithelial marker E‐cadherin and the decreased expression of mesenchymal marker vimentin by Western blot analysis, reverse transcription PCR analysis, and immunofluorescence analysis. Consistent with these observations, the repression of FOXJ2 in weakly metastatic MCF‐7 cells remarkably promoted cellular motility. Our study demonstrates that FOXJ2 can inhibit the metastasis of human breast cancer by regulating the EMT key markers E‐cadherin and vimentin. J. Cell. Biochem. 113: 2729–2737, 2012. © 2012 Wiley Periodicals, Inc.