Molecular mechanisms underlying pentabrominated diphenyl ether-induced proliferation in breast cancer MCF-7 cells
Yan‐Hong Cui, Ping Zhan, Dong Luo, Yinyin Xia
Abstract
Yan‐Hong Cui, Ping Zhan, Dong Luo, Yinyin Xia
Abstract
The effects of pentabrominated diphenyl ethers (BDE-99) were examined on mRNA and protein expressions of c-Myc and p53 in breast cancer MCF-7 cells. Human breast cancer MCF-7 cells were cultured in Dulbecco's modified Eagle's medium. 3-[4,5-Dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) assay was employed to investigate cell proliferation. Real time-polymerase chain reaction (RT-PCR) and immunohistochemistry were performed to detect mRNA and protein expressions of c-Myc and p53. At the concentration of 1 × (10−4–10−8) mol L−1, BDE-99 stimulated proliferation of MCF-7 cells in a concentration- and time-dependent manner. RT-PCR and immunohistochemistry analyses revealed that treatment with 1 × (10−4–10−7) mol L−1 for 72 h resulted in significantly increased mRNA and protein expressions of c-Myc and inhibited p53. It is possible that BDE-99 exerted estrogenic actions and might markedly stimulate proliferation in estrogen responsive breast cancer MCF-7 cells. BDE-99 similar to estrogen promoted c-Myc mRNA and protein, and inhibited p53 mRNA and protein expression in MCF-7 cell.
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The effects of pentabrominated diphenyl ethers (BDE-99) were examined on mRNA and protein expressions of c-Myc and p53 in breast cancer MCF-7 cells. Human breast cancer MCF-7 cells were cultured in Dulbecco's modified Eagle's medium. 3-[4,5-Dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) assay was employed to investigate cell proliferation. Real time-polymerase chain reaction (RT-PCR) and immunohistochemistry were performed to detect mRNA and protein expressions of c-Myc and p53. At the concentration of 1 × (10−4–10−8) mol L−1, BDE-99 stimulated proliferation of MCF-7 cells in a concentration- and time-dependent manner. RT-PCR and immunohistochemistry analyses revealed that treatment with 1 × (10−4–10−7) mol L−1 for 72 h resulted in significantly increased mRNA and protein expressions of c-Myc and inhibited p53. It is possible that BDE-99 exerted estrogenic actions and might markedly stimulate proliferation in estrogen responsive breast cancer MCF-7 cells. BDE-99 similar to estrogen promoted c-Myc mRNA and protein, and inhibited p53 mRNA and protein expression in MCF-7 cell.
Key concepts: MCF-7, Messenger RNA, Cell growth, Immunohistochemistry, Estrogen, Chemistry, Molecular biology, Breast cancer