Open AccessTP53I11 suppresses epithelial-mesenchymal transition and metastasis of breast cancer cells
Author(s) -
Tongqian Xiao,
Zhongjuan Xu,
Hai Zhang,
Junsa Geng,
Yong Qiao,
Yu Liang,
Yanzhen Yu,
Qun Dong,
Guangli Suo
Publication year - 2019
Publication title -
bmb reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.511
H-Index - 77
eISSN - 1976-670X
pISSN - 1976-6696
DOI - 10.5483/bmbrep.2019.52.6.173
Subject(s) - epithelial–mesenchymal transition , metastasis , anoikis , cancer research , downregulation and upregulation , breast cancer , cancer cell , breast cancer metastasis , snai1 , mesenchymal stem cell , regulator , hypoxia (environmental) , cancer , biology , chemistry , medicine , cancer metastasis , pathology , gene , biochemistry , organic chemistry , oxygen
Epithelial-mesenchymal transition (EMT) is widely-considered to be a modulating factor of anoikis and cancer metastasis. We found that, in MDA-MB-231 cells, TP53I11 (tumor protein P53 inducible protein 11) suppressed EMT and migration in vitro, and inhibited metastasis in vivo. Our findings showed that hypoxic treatment upregulated the expression of HIF1α, but reduced TP53I11 protein levels and TP53I11 overexpression reduced HIF1α expression under normal culture and hypoxicconditions, and in xenografts of MDA-MB-231 cells. Considering HIF1α is a master regulator of the hypoxic response and that hypoxia is a crucial trigger of cancer metastasis, our study suggests that TP53I11 may suppress EMT and metastasis by reducing HIF1α protein levels in breast cancer cells.
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