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TP53I11 Suppresses Epithelial-mesenchymal Transition and Metastasis of Breast Cancer Cells
Tongqian Xiao1,2, Zhongjuan Xu1, Hai Zhang1, Junsa Geng1,4, Yong Qiao1, Yu Liang1,3, Yanzhen Yu1,4, Qun Dong5, Guangli Suo1,*
1CAS Key Laboratory of Nano-Bio Interface, Suzhou Institute of Nano-Tech and Nano-Bionics, Chinese Academy of Sciences,
2Suzhou Institute of Nano-Tech and Nano-Bionics, University of Chinese Academy of Sciences,
3School of Life Sciences, Shanghai University,
4Suzhou Institute of Nano-Tech and Nano-Bionics, University of Science and Technology of China,
5Pathology Department, Taikang Xianlin Drum Tower Hospital
Abstract
Epithelial-mesenchymal transition (EMT) was widely considered a modulating factor for anoikis and cancer metastasis. We found that, in MDA-MB-231 cells, TP53I11 (Tumor Protein P53 Inducible Protein 11) suppressed the EMT and migration in vitro, and inhibited metastasis in vivo. Our findings showed that hypoxia treatment upregulated the expression of HIF1メ but reduced TP53I11 protein level, and TP53I11 overexpression reduced the HIF1メ expression levels under normal culture, hypoxia treatment and in xenograft of MDA-MB-231 cells. Considering HIF1メ is a master regulator of the hypoxic response and hypoxia is a crucial inducement triggering cancer metastasis, our study suggests that TP53I11 may suppress EMT and metastasis by reducing HIF1メ protein level in breast cancer cells.
Abstract, Accepted Manuscript(in press) [Submitted on July 24, 2018, Accepted on October 2, 2018]
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