2015The FASEB JournalRequires access

MED28 Modulates Cell Cycle Progression in Human Breast Cancer Cells

Chun‐I Li, Nien‐Tsu Hsieh, Chun‐Yin Huang, Hsueh‐Chen Chang, Ming‐Fen Lee

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Abstract

Mediator subunit MED28 is found highly expressed in several types of tumor including breast cancer. Previously we have reported that MED28 regulates cellular migration and functions as an upstream regulator of the NFkB/MMP9 axis upon EGF stimulationin human breast cancer cells. In the current study we investigated the effect of MED28 on cell growth in human breast cancer cells. Suppression of MED28 expression inhibited cell growth accompanied by lowering the expression of p‐RelA/p65, cyclin D1, and p‐pRb as well as the transcriptional activity of NFkB, but increasing the expression of FOXO3a and p27. Overexpression of MED28 promoted G1 to S transition and, thereby, stimulated cell growth. Our data indicate that MED28 modulates cell growth through FOXO3a and NFkB in human breast cancer cells. Not only is MED28 involved in cellular migration and invasion but also cell cycle progression in human breast cancer cells, reiterating the significance of this multifaceted protein in breast cancer. (This work was supported by the grants NSC101‐2320‐B‐309‐001 and NSC102‐2320‐B‐309‐001‐MY3 to M‐F Lee.)

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What this paper is about

Mediator subunit MED28 is found highly expressed in several types of tumor including breast cancer. Previously we have reported that MED28 regulates cellular migration and functions as an upstream regulator of the NFkB/MMP9 axis upon EGF stimulationin human breast cancer cells. In the current study we investigated the effect of MED28 on cell growth in human breast cancer cells. Suppression of MED28 expression inhibited cell growth accompanied by lowering the expression of p‐RelA/p65, cyclin D1, and p‐pRb as well as the transcriptional activity of NFkB, but increasing the expression of FOXO3a and p27. Overexpression of MED28 promoted G1 to S transition and, thereby, stimulated cell growth. Our data indicate that MED28 modulates cell growth through FOXO3a and NFkB in human breast cancer cells. Not only is MED28 involved in cellular migration and invasion but also cell cycle progression in human breast cancer cells, reiterating the significance of this multifaceted protein in breast cancer. (This work was supported by the grants NSC101‐2320‐B‐309‐001 and NSC102‐2320‐B‐309‐001‐MY3 to M‐F Lee.)

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Available abstract

Mediator subunit MED28 is found highly expressed in several types of tumor including breast cancer. Previously we have reported that MED28 regulates cellular migration and functions as an upstream regulator of the NFkB/MMP9 axis upon EGF stimulationin human breast cancer cells. In the current study we investigated the effect of MED28 on cell growth in human breast cancer cells. Suppression of MED28 expression inhibited cell growth accompanied by lowering the expression of p‐RelA/p65, cyclin D1, and p‐pRb as well as the transcriptional activity of NFkB, but increasing the expression of FOXO3a and p27. Overexpression of MED28 promoted G1 to S transition and, thereby, stimulated cell growth. Our data indicate that MED28 modulates cell growth through FOXO3a and NFkB in human breast cancer cells. Not only is MED28 involved in cellular migration and invasion but also cell cycle progression in human breast cancer cells, reiterating the significance of this multifaceted protein in breast cancer. (This work was supported by the grants NSC101‐2320‐B‐309‐001 and NSC102‐2320‐B‐309‐001‐MY3 to M‐F Lee.)

Key concepts: Cyclin D1, Cell growth, Cancer research, Breast cancer, Cell cycle, Cancer cell, Cancer, Regulator

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