Abstract
Mediator complex subunit MED23 has been reported to facilitate the transformation induced by oncogenic Ras in non-small-cell lung carcinoma (NSCLC). However, the expression pattern and biological functions of MED23 in the progression of NSCLC are not fully understood. In this study, it was found that the expression of MED23 was significantly upregulated in NSCLC samples compared to their adjacent normal tissues. Moreover, in the biological function studies, overexpression of MED23 was further validated to promote the growth, migration, and metastasis of NSCLC cells, while knockdown of the expression of MED23 inhibited the growth, migration, and metastasis of NSCLC cells in vitro and in vivo. Mechanistically, MED23 was found to interact with beta-catenin and activate beta-catenin/TCF signaling. Our study demonstrated that MED23 played an oncogenic role in the progression of NSCLC and that MED23 might be a promising target for the treatment of NSCLC.
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This work was supported by the National Natural Science Foundation of China (81201840), the Natural Science Foundation of Shanghai (13ZR1461300), the Health Bureau Foundation of Shanghai (20124Y152), and Chenxing Young Scholarship of Shanghai Jiaotong University.
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Jianxin Shi and Hongcheng Liu contributed equally to this work.
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Shi, J., Liu, H., Yao, F. et al. Upregulation of mediator MED23 in non-small-cell lung cancer promotes the growth, migration, and metastasis of cancer cells. Tumor Biol. 35, 12005–12013 (2014). https://doi.org/10.1007/s13277-014-2499-3
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DOI: https://doi.org/10.1007/s13277-014-2499-3