MED28 Regulates Epithelial–Mesenchymal Transition Through NFκB in Human Breast Cancer Cells

Chun Yin Huang, Nien Tsu Hsieh, Chun I. Li, Yu Ting Weng, Hsiao-Sheng Liu, Ming Fen Lee

研究成果: Article

6 引文 (Scopus)

摘要

MED28, a mammalian Mediator subunit, was found highly expressed in several types of malignancy, including breast cancer. Recently, we have identified a role of MED28 in regulating both cell growth and migration in human breast cancer cells. In epithelium-derived solid tumor, migration and invasion are preceded by the progression of epithelial–mesenchymal transition (EMT) which calls for downregulation of epithelial markers as well as upregulation of mesenchymal markers, among other features. The objective of this study was to investigate a putative role of MED28 in the progression of EMT in human breast cancer cells. In fibroblast-like MDA-MB-231 cells, suppression of MED28 attenuated the mesenchymal morphology, concomitantly with a reduction of several mesenchymal biomarkers and Snail, a transcriptional repressor of E-cadherin. The suppression effect was also accompanied by downregulation of p-NFκB/p65. However, overexpression of MED28 exhibited in an opposite manner. In epithelial MCF7 cells, administration of Adriamycin®, an experimental EMT induction system, led to a mesenchyme-like appearance correlated with increased expression of MED28, p-p65, and Snail, and a reciprocal change of epithelial and mesenchymal markers. Furthermore, suppression of MED28 attenuated the experimental EMT effect and restored the original expression status of E-cadherin and MMP9 in MCF7 cells. Our data indicate that MED28 modulates the development of EMT through NFκB in human breast cancer cells, further reinforcing the significance of MED28 in the progression of breast cancer on top of its role in cell growth and migration. J. Cell. Physiol. 232: 1337–1345, 2017.

原文English
頁(從 - 到)1337-1345
頁數9
期刊Journal of Cellular Physiology
232
發行號6
DOIs
出版狀態Published - 2017 六月 1

指紋

Cells
Cell growth
Cadherins
Breast Neoplasms
MCF-7 Cells
Cell Movement
Biomarkers
Fibroblasts
Down-Regulation
Doxorubicin
Tumors
Mesoderm
Growth
Neoplasms
Up-Regulation
Epithelium
Epithelial Cells

All Science Journal Classification (ASJC) codes

  • Physiology
  • Clinical Biochemistry
  • Cell Biology

引用此文

Huang, C. Y., Hsieh, N. T., Li, C. I., Weng, Y. T., Liu, H-S., & Lee, M. F. (2017). MED28 Regulates Epithelial–Mesenchymal Transition Through NFκB in Human Breast Cancer Cells. Journal of Cellular Physiology, 232(6), 1337-1345. https://doi.org/10.1002/jcp.25610
Huang, Chun Yin ; Hsieh, Nien Tsu ; Li, Chun I. ; Weng, Yu Ting ; Liu, Hsiao-Sheng ; Lee, Ming Fen. / MED28 Regulates Epithelial–Mesenchymal Transition Through NFκB in Human Breast Cancer Cells. 於: Journal of Cellular Physiology. 2017 ; 卷 232, 編號 6. 頁 1337-1345.
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abstract = "MED28, a mammalian Mediator subunit, was found highly expressed in several types of malignancy, including breast cancer. Recently, we have identified a role of MED28 in regulating both cell growth and migration in human breast cancer cells. In epithelium-derived solid tumor, migration and invasion are preceded by the progression of epithelial–mesenchymal transition (EMT) which calls for downregulation of epithelial markers as well as upregulation of mesenchymal markers, among other features. The objective of this study was to investigate a putative role of MED28 in the progression of EMT in human breast cancer cells. In fibroblast-like MDA-MB-231 cells, suppression of MED28 attenuated the mesenchymal morphology, concomitantly with a reduction of several mesenchymal biomarkers and Snail, a transcriptional repressor of E-cadherin. The suppression effect was also accompanied by downregulation of p-NFκB/p65. However, overexpression of MED28 exhibited in an opposite manner. In epithelial MCF7 cells, administration of Adriamycin{\circledR}, an experimental EMT induction system, led to a mesenchyme-like appearance correlated with increased expression of MED28, p-p65, and Snail, and a reciprocal change of epithelial and mesenchymal markers. Furthermore, suppression of MED28 attenuated the experimental EMT effect and restored the original expression status of E-cadherin and MMP9 in MCF7 cells. Our data indicate that MED28 modulates the development of EMT through NFκB in human breast cancer cells, further reinforcing the significance of MED28 in the progression of breast cancer on top of its role in cell growth and migration. J. Cell. Physiol. 232: 1337–1345, 2017.",
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Huang, CY, Hsieh, NT, Li, CI, Weng, YT, Liu, H-S & Lee, MF 2017, 'MED28 Regulates Epithelial–Mesenchymal Transition Through NFκB in Human Breast Cancer Cells', Journal of Cellular Physiology, 卷 232, 編號 6, 頁 1337-1345. https://doi.org/10.1002/jcp.25610

MED28 Regulates Epithelial–Mesenchymal Transition Through NFκB in Human Breast Cancer Cells. / Huang, Chun Yin; Hsieh, Nien Tsu; Li, Chun I.; Weng, Yu Ting; Liu, Hsiao-Sheng; Lee, Ming Fen.

於: Journal of Cellular Physiology, 卷 232, 編號 6, 01.06.2017, p. 1337-1345.

研究成果: Article

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T1 - MED28 Regulates Epithelial–Mesenchymal Transition Through NFκB in Human Breast Cancer Cells

AU - Huang, Chun Yin

AU - Hsieh, Nien Tsu

AU - Li, Chun I.

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AU - Liu, Hsiao-Sheng

AU - Lee, Ming Fen

PY - 2017/6/1

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N2 - MED28, a mammalian Mediator subunit, was found highly expressed in several types of malignancy, including breast cancer. Recently, we have identified a role of MED28 in regulating both cell growth and migration in human breast cancer cells. In epithelium-derived solid tumor, migration and invasion are preceded by the progression of epithelial–mesenchymal transition (EMT) which calls for downregulation of epithelial markers as well as upregulation of mesenchymal markers, among other features. The objective of this study was to investigate a putative role of MED28 in the progression of EMT in human breast cancer cells. In fibroblast-like MDA-MB-231 cells, suppression of MED28 attenuated the mesenchymal morphology, concomitantly with a reduction of several mesenchymal biomarkers and Snail, a transcriptional repressor of E-cadherin. The suppression effect was also accompanied by downregulation of p-NFκB/p65. However, overexpression of MED28 exhibited in an opposite manner. In epithelial MCF7 cells, administration of Adriamycin®, an experimental EMT induction system, led to a mesenchyme-like appearance correlated with increased expression of MED28, p-p65, and Snail, and a reciprocal change of epithelial and mesenchymal markers. Furthermore, suppression of MED28 attenuated the experimental EMT effect and restored the original expression status of E-cadherin and MMP9 in MCF7 cells. Our data indicate that MED28 modulates the development of EMT through NFκB in human breast cancer cells, further reinforcing the significance of MED28 in the progression of breast cancer on top of its role in cell growth and migration. J. Cell. Physiol. 232: 1337–1345, 2017.

AB - MED28, a mammalian Mediator subunit, was found highly expressed in several types of malignancy, including breast cancer. Recently, we have identified a role of MED28 in regulating both cell growth and migration in human breast cancer cells. In epithelium-derived solid tumor, migration and invasion are preceded by the progression of epithelial–mesenchymal transition (EMT) which calls for downregulation of epithelial markers as well as upregulation of mesenchymal markers, among other features. The objective of this study was to investigate a putative role of MED28 in the progression of EMT in human breast cancer cells. In fibroblast-like MDA-MB-231 cells, suppression of MED28 attenuated the mesenchymal morphology, concomitantly with a reduction of several mesenchymal biomarkers and Snail, a transcriptional repressor of E-cadherin. The suppression effect was also accompanied by downregulation of p-NFκB/p65. However, overexpression of MED28 exhibited in an opposite manner. In epithelial MCF7 cells, administration of Adriamycin®, an experimental EMT induction system, led to a mesenchyme-like appearance correlated with increased expression of MED28, p-p65, and Snail, and a reciprocal change of epithelial and mesenchymal markers. Furthermore, suppression of MED28 attenuated the experimental EMT effect and restored the original expression status of E-cadherin and MMP9 in MCF7 cells. Our data indicate that MED28 modulates the development of EMT through NFκB in human breast cancer cells, further reinforcing the significance of MED28 in the progression of breast cancer on top of its role in cell growth and migration. J. Cell. Physiol. 232: 1337–1345, 2017.

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