TP53I11 suppresses epithelial-mesenchymal transition and metastasis of breast cancer cells
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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 HIF1, but reduced TP53I11 protein levels and TP53I11 overexpression reduced HIF1 expression under normal culture and hypoxicconditions, and in xenografts of MDA-MB-231 cells. Considering HIF1 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 HIF1 protein levels in breast cancer cells.
Abstract
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 HIF1, but reduced TP53I11 protein levels and TP53I11 overexpression reduced HIF1 expression under normal culture and hypoxicconditions, and in xenografts of MDA-MB-231 cells. Considering HIF1 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 HIF1 protein levels in breast cancer cells.
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