Resveratrol and pterostilbene regulate MED28 (magicin/EG1) expression and cell growth in MCF7 human breast cancer cells

Huang, Chun‐Yin; Hsieh, Nien-Tsu; Pan, Min‐Hsiung; Li, Chun‐I; Chou, Yu-Hsuan; Chiou, Yi-Siou; Lee, Ming‐Fen

doi:10.1016/j.jff.2014.11.006

Cited by 6 publications

(20 citation statements)

References 43 publications

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“…In addition to NSCLC, our group has previously identified a role of MED28 in the malignancy of breast cancer as indicated by its effect on migration and invasion, as well as cell morphology of human breast cancer cells (Huang et al, ; Huang et al, ). Moreover, we have also reported that MED28 is involved in cell growth in both human breast cancer cells and colorectal cancer cells (Huang et al, ; Lee et al, ). Our findings further emphasize the significance of MED28 and imply the prospective translational application of MED28 in tumorigenesis and cancer development.…”

Section: Discussionmentioning

confidence: 83%

“…We also have reported that MED28 enhanced epidermal growth factor-induced migration by upregulating the expression of MMP9 in MDA-MB-231 human breast cancer cells . It appears that MED28 directly mediates MMP2 activation Both MED28 and FOXM1 can modulate cell growth (Huang et al, 2015;Lee et al, 2016;Wang et al, 2005;Wierstra, 2013), and this role may affect the cell numbers after knockdown or overexpression.…”

Section: Suppression Of Med28 Blocked Cellular Migration and Invasionmentioning

confidence: 99%

“…For example, the expression of Mediator subunit MED15 with its clinical implications in head and neck squamous cell carcinoma has been identified (Shaikhibrahim et al, ). Recently, we have reported that MED28, another Mediator subunit, is involved in cell growth in human breast cancer cells and colorectal cancer cells (Huang et al, ; Lee, Hsieh, Huang, & Li, ). Therefore, mammalian Mediator subunits display novel cellular roles in addition to their function in transcriptional activation.…”

Section: Introductionmentioning

confidence: 99%

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MED28 and forkhead box M1 (FOXM1) mediate matrix metalloproteinase 2 (MMP2)‐dependent cellular migration in human nonsmall cell lung cancer (NSCLC) cells

Hsieh

Huang

et al. 2018

Journal Cellular Physiology

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Non‐small‐cell lung cancer (NSCLC) accounts for the majority of the lung cancer cases that have become a leading cause of cancer deaths worldwide. Overexpression of transcription factor forkhead box M1 (FOXM1) is involved in the inauspicious development of several types of cancer, including lung tumor aggressiveness. Our laboratory has previously found that MED28, a Mediator subunit for transcriptional activation, modulates cell growth, epithelial‐mesenchymal transition, migration, and invasion in human breast cancer cells. The objective of the current study is to investigate the potential role of MED28 and FOXM1 in NSCLC. In addition to A549 and PC9 cells, we also used a doxycycline‐inducible system to generate FOXM1‐overexpressed A549‐DN cells, and we explored the connection of MED28 with FOXM1 and their effect on migration. Herein, we report that the increased expression levels of both MED28 and FOXM1 elevated the expression of matrix metalloproteinase 2 (MMP2), a metastasis marker, which enhanced cell migration and matrigel invasion of NSCLC cells. Furthermore, MED28 interacted with FOXM1, and both exhibited a mutual effect on the expression and subcellular localization. Moreover, MED28 small interfering RNA‐mediated MMP2 gene suppression could be attenuated by inducible expression of a constitutively active form of FOXM1, which consequently restored the migration and invasion ability of NSCLC cells. Our data indicate that MED28 interacts with FOXM1, and each affects the expression and localization of the other, and, more importantly, both regulate MMP2‐dependent migration and invasion in human lung cancer cells.

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Section: Discussionmentioning

confidence: 83%

Section: Suppression Of Med28 Blocked Cellular Migration and Invasionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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MED28 and forkhead box M1 (FOXM1) mediate matrix metalloproteinase 2 (MMP2)‐dependent cellular migration in human nonsmall cell lung cancer (NSCLC) cells

Hsieh

Huang

et al. 2018

Journal Cellular Physiology

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“…In conclusion, ATRA could facilitate the maintenance of epithelial integrity and, meanwhile, inhibit cell growth by suppressing MED28 and upregulating E‐cadherin and HBP1in human colorectal cancer cells. Previously, we found that MED28 is involved in cell growth, migration, and invasion in human breast cancer cells (Lee et al, ; Huang et al, , ). Our current data further strengthens the role of MED28 in cell growth in the development of cancer.…”

Section: Discussionmentioning

confidence: 90%

“…Recent literature has indicated that several Mediator subunits, including CDK8, MED12, and MED1 are involved in cancer development (Kim et al, ; Vijayvargia et al, ; Firestein et al, ). Our laboratory has also reported that MED28 regulates cell growth and migration in human breast cancer cells (Lee et al, ; Huang et al, , ). Moreover, MED28 was found highly expressed in breast, colorectal, and prostate cancers (Zhang et al, ), indicating MED28 could also be involved in colorectal cancer.…”

mentioning

confidence: 89%

AllTrans-Retinoic Acid Mediates MED28/HMG Box-Containing Protein 1 (HBP1)/β-Catenin Signaling in Human Colorectal Cancer Cells

et al. 2015

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Vitamin A is required for normal body function, including vision, epithelial integrity, growth, and differentiation. All trans-retinoic acid (ATRA), a family member of vitamin A, has been explored in treating acute promyelocytic leukemia and other types of cancer. Dysregulated Wnt/β-catenin signaling and disrupted cadherin-catenin complex often contribute to colorectal malignancy. MED28, a mammalian Mediator subunit, is found highly expressed in breast and colorectal cancers. Our laboratory has also reported that MED28 regulates cell growth, migration, and invasion in human breast cancer cells. In the current study we investigated the effect of ATRA on MED28 and Wnt/β-catenin signaling in colorectal cancer. HCT116, HT29, SW480, and SW620, four human colorectal cancer cell lines representing different stages of carcinogenesis and harboring critical genetic changes, were employed. Our data indicated that regardless of genetic variations among these cells, suppression of MED28 reduced the expression of cyclin D1, c-Myc, and nuclear β-catenin, but increased the expression of E-cadherin and HMG box-containing protein 1 (HBP1) where HBP1 has been described as a negative regulator of the Wnt/β-catenin signaling. The reporter activity of an HBP1 promoter increased upon MED28 knockdown, but decreased upon MED28 overexpression. ATRA reduced the expression of MED28 and mimicked the effect of MED28 suppression in down-regulating Wnt/β-catenin signaling. Taken together, ATRA can reverse the suppressive effect of MED28 on HBP1 and E-cadherin and inactivate the Wnt/β-catenin pathway in colorectal cancer, suggesting a protective effect of ATRA against colorectal cancer. J. Cell. Physiol. 231: 1796-1803, 2016. © 2015 Wiley Periodicals, Inc.

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

Huang

Hsieh

et al. 2016

Journal Cellular Physiology

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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. © 2016 Wiley Periodicals, Inc.

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Resveratrol and pterostilbene regulate MED28 (magicin/EG1) expression and cell growth in MCF7 human breast cancer cells

Cited by 6 publications

References 43 publications

MED28 and forkhead box M1 (FOXM1) mediate matrix metalloproteinase 2 (MMP2)‐dependent cellular migration in human nonsmall cell lung cancer (NSCLC) cells

MED28 and forkhead box M1 (FOXM1) mediate matrix metalloproteinase 2 (MMP2)‐dependent cellular migration in human nonsmall cell lung cancer (NSCLC) cells

AllTrans-Retinoic Acid Mediates MED28/HMG Box-Containing Protein 1 (HBP1)/β-Catenin Signaling in Human Colorectal Cancer Cells

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

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