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Serum deprivation response inhibits breast cancer progression by blocking transforming growth factor-β signaling.

Tian Y, Yu Y, Hou LK, Chi JR, Mao JF, Xia L, Wang X, Wang P, Cao XC - Cancer Sci. (2016)

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.

View Article: PubMed Central - PubMed

Affiliation: The First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, China.

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Serum deprivation response (SDPR) depletion is linked to the epithelial–mesenchymal transition (EMT)‐like phenotype. (a) Cellular morphology of the SDPR‐overexpressed MDA‐MB‐231 (upper), SDPR‐depleted MCF10A (lower), or appropriate control cells. (b–d) RT‐qPCR analysis of mRNA expression of the mesenchymal markers Vimentin and N‐cadherin (CDH2), and epithelial markers E‐cadherin (CDH1) and β‐catenin (CTNNB1) in the SDPR‐overexpressed MDA‐MB‐231 (a), SDPR‐depleted MCF10A (b) or appropriate control cells. (d) Western blot analysis of protein expression of the mesenchymal markers Vimentin and N‐cadherin, and epithelial markers E‐cadherin and β‐catenin in the SDPR‐overexpressed MDA‐MB‐231 (left) SDPR‐depleted MCF10A (right), or appropriate control cells. (e) The cell cycle distribution of SDPR‐overexpressed MDA‐MB‐231 (upper) SDPR‐depleted MCF10A (lower), or appropriate control cells was analyzed by flow cytometry analysis. (f) Western blot analysis of protein expression of the Cyclin D1 and p21 in cells treated in (e). *P < 0.05, ***P < 0.001.
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cas12879-fig-0004: Serum deprivation response (SDPR) depletion is linked to the epithelial–mesenchymal transition (EMT)‐like phenotype. (a) Cellular morphology of the SDPR‐overexpressed MDA‐MB‐231 (upper), SDPR‐depleted MCF10A (lower), or appropriate control cells. (b–d) RT‐qPCR analysis of mRNA expression of the mesenchymal markers Vimentin and N‐cadherin (CDH2), and epithelial markers E‐cadherin (CDH1) and β‐catenin (CTNNB1) in the SDPR‐overexpressed MDA‐MB‐231 (a), SDPR‐depleted MCF10A (b) or appropriate control cells. (d) Western blot analysis of protein expression of the mesenchymal markers Vimentin and N‐cadherin, and epithelial markers E‐cadherin and β‐catenin in the SDPR‐overexpressed MDA‐MB‐231 (left) SDPR‐depleted MCF10A (right), or appropriate control cells. (e) The cell cycle distribution of SDPR‐overexpressed MDA‐MB‐231 (upper) SDPR‐depleted MCF10A (lower), or appropriate control cells was analyzed by flow cytometry analysis. (f) Western blot analysis of protein expression of the Cyclin D1 and p21 in cells treated in (e). *P < 0.05, ***P < 0.001.

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.


Serum deprivation response inhibits breast cancer progression by blocking transforming growth factor-β signaling.

Tian Y, Yu Y, Hou LK, Chi JR, Mao JF, Xia L, Wang X, Wang P, Cao XC - Cancer Sci. (2016)

Serum deprivation response (SDPR) depletion is linked to the epithelial–mesenchymal transition (EMT)‐like phenotype. (a) Cellular morphology of the SDPR‐overexpressed MDA‐MB‐231 (upper), SDPR‐depleted MCF10A (lower), or appropriate control cells. (b–d) RT‐qPCR analysis of mRNA expression of the mesenchymal markers Vimentin and N‐cadherin (CDH2), and epithelial markers E‐cadherin (CDH1) and β‐catenin (CTNNB1) in the SDPR‐overexpressed MDA‐MB‐231 (a), SDPR‐depleted MCF10A (b) or appropriate control cells. (d) Western blot analysis of protein expression of the mesenchymal markers Vimentin and N‐cadherin, and epithelial markers E‐cadherin and β‐catenin in the SDPR‐overexpressed MDA‐MB‐231 (left) SDPR‐depleted MCF10A (right), or appropriate control cells. (e) The cell cycle distribution of SDPR‐overexpressed MDA‐MB‐231 (upper) SDPR‐depleted MCF10A (lower), or appropriate control cells was analyzed by flow cytometry analysis. (f) Western blot analysis of protein expression of the Cyclin D1 and p21 in cells treated in (e). *P < 0.05, ***P < 0.001.
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cas12879-fig-0004: Serum deprivation response (SDPR) depletion is linked to the epithelial–mesenchymal transition (EMT)‐like phenotype. (a) Cellular morphology of the SDPR‐overexpressed MDA‐MB‐231 (upper), SDPR‐depleted MCF10A (lower), or appropriate control cells. (b–d) RT‐qPCR analysis of mRNA expression of the mesenchymal markers Vimentin and N‐cadherin (CDH2), and epithelial markers E‐cadherin (CDH1) and β‐catenin (CTNNB1) in the SDPR‐overexpressed MDA‐MB‐231 (a), SDPR‐depleted MCF10A (b) or appropriate control cells. (d) Western blot analysis of protein expression of the mesenchymal markers Vimentin and N‐cadherin, and epithelial markers E‐cadherin and β‐catenin in the SDPR‐overexpressed MDA‐MB‐231 (left) SDPR‐depleted MCF10A (right), or appropriate control cells. (e) The cell cycle distribution of SDPR‐overexpressed MDA‐MB‐231 (upper) SDPR‐depleted MCF10A (lower), or appropriate control cells was analyzed by flow cytometry analysis. (f) Western blot analysis of protein expression of the Cyclin D1 and p21 in cells treated in (e). *P < 0.05, ***P < 0.001.
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.

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.

View Article: PubMed Central - PubMed

Affiliation: The First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, China.

Show MeSH
Related in: MedlinePlus