Serum deprivation response inhibits breast cancer progression by blocking transforming growth factor-β signaling.
Bottom Line: Here, we found that SDPR is downregulated in human breast cancer.In conclusion, our results showed that SDPR inhibits breast cancer progression by blocking TGF-β signaling.SDPR depletion induces epithelial-mesenchymal transition by activation of TGF-β signaling.
Affiliation: The First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, China.Show MeSH
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Mentions: Epithelial–mesenchymal transition enables epithelial cells to acquire an invasive mesenchymal phenotype and is a critical mechanism for the initial step of metastasis.12 We observed that MDA‐MB‐231 cells transfected with vector control retained their fibroblast‐like morphology, whereas SDPR‐overexpressed cells displayed a cobblestone‐like morphology (Fig. 4a; upper). Compared with the siControl cells, SDPR depletion transformed MCF10A cells from a typical epithelial morphology into fibroblast‐like shape (Fig. 4a; lower). To examine the effect of SDPR expression in breast cancer EMT, we measured the expression of epithelial and mesenchymal markers by RT‐qPCR and western blot. SDPR‐overexpressed MDA‐MB‐231 cells exhibited a significant downregulation of vimentin and N‐cadherin (CDH2), while the epithelial markers E‐cadherin (CDH1) and β‐catenin (CTNNB1) were dramatically decreased by RT‐qPCR (Fig. 4b) and western blot (Fig. 4d; left). In contrast, the vimentin and CDH2 was upregulated, while the CDH1 and CTNNB1 was downregulated in SDPR‐depleted MCF10A cells by RT‐qPCR (Fig. 4c) and western blot (Fig. 4d; right). These results showed that SDPR inhibits EMT‐like phenotype in breast cancer cells.
Affiliation: The First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, China.