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Article

SETDB1 induces epithelial‑mesenchymal transition in breast carcinoma by directly binding with Snail promoter

  • Authors:
    • Wenlin Yang
    • Ying Su
    • Chenjian Hou
    • Linlin Chen
    • Danmei Zhou
    • Kehan Ren
    • Zhaoping Zhou
    • Renya Zhang
    • Xiuping Liu
  • View Affiliations / Copyright

    Affiliations: Department of Pathology, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, Shandong 272029, P.R. China, Department of Pathology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, P.R. China, Department of Pathology, The Fifth Hospital of Shanghai, Fudan University, Shanghai 200240, P.R. China, Department of General Surgery, Huashan Hospital, Fudan University School of Medicine, Shanghai 200040, P.R. China
  • Pages: 1284-1292
    |
    Published online on: November 19, 2018
       https://doi.org/10.3892/or.2018.6871
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Abstract

SET domain bifurcated 1 (SETDB1) is a histone H3 lysine 9 methyltransferase that is highly expressed in various tumor types, including breast cancer. However, how SETDB1 functions in breast cancer is unclear. In the present study, proliferation, migration and invasion assays were performed to explore the role of SETDB1 in breast cancer cells. SETDB1 downregulation in BT549 and MDA‑MB‑231 cells reduced cell proliferation, whereas upregulation in MCF7 and T47D cells enhanced proliferation. Depletion of SETDB1 suppressed cell migration and invasion in vitro and reduced lung metastasis in vivo. By contrast, SETDB1 overexpression enhanced cell migration and invasiveness. Notably, SETDB1 overexpression appeared to induce epithelial‑mesenchymal transition (EMT) in MCF7 cells. Mechanistic investigations indicated that SETDB1 acts as an EMT inducer by binding directly to the promoter of the transcription factor Snail. Thus, SETDB1 is involved in breast cancer metastasis and may be a therapeutic target for treating patients with breast cancer.
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Copy and paste a formatted citation
Spandidos Publications style
Yang W, Su Y, Hou C, Chen L, Zhou D, Ren K, Zhou Z, Zhang R and Liu X: SETDB1 induces epithelial‑mesenchymal transition in breast carcinoma by directly binding with Snail promoter. Oncol Rep 41: 1284-1292, 2019.
APA
Yang, W., Su, Y., Hou, C., Chen, L., Zhou, D., Ren, K. ... Liu, X. (2019). SETDB1 induces epithelial‑mesenchymal transition in breast carcinoma by directly binding with Snail promoter. Oncology Reports, 41, 1284-1292. https://doi.org/10.3892/or.2018.6871
MLA
Yang, W., Su, Y., Hou, C., Chen, L., Zhou, D., Ren, K., Zhou, Z., Zhang, R., Liu, X."SETDB1 induces epithelial‑mesenchymal transition in breast carcinoma by directly binding with Snail promoter". Oncology Reports 41.2 (2019): 1284-1292.
Chicago
Yang, W., Su, Y., Hou, C., Chen, L., Zhou, D., Ren, K., Zhou, Z., Zhang, R., Liu, X."SETDB1 induces epithelial‑mesenchymal transition in breast carcinoma by directly binding with Snail promoter". Oncology Reports 41, no. 2 (2019): 1284-1292. https://doi.org/10.3892/or.2018.6871
Copy and paste a formatted citation
x
Spandidos Publications style
Yang W, Su Y, Hou C, Chen L, Zhou D, Ren K, Zhou Z, Zhang R and Liu X: SETDB1 induces epithelial‑mesenchymal transition in breast carcinoma by directly binding with Snail promoter. Oncol Rep 41: 1284-1292, 2019.
APA
Yang, W., Su, Y., Hou, C., Chen, L., Zhou, D., Ren, K. ... Liu, X. (2019). SETDB1 induces epithelial‑mesenchymal transition in breast carcinoma by directly binding with Snail promoter. Oncology Reports, 41, 1284-1292. https://doi.org/10.3892/or.2018.6871
MLA
Yang, W., Su, Y., Hou, C., Chen, L., Zhou, D., Ren, K., Zhou, Z., Zhang, R., Liu, X."SETDB1 induces epithelial‑mesenchymal transition in breast carcinoma by directly binding with Snail promoter". Oncology Reports 41.2 (2019): 1284-1292.
Chicago
Yang, W., Su, Y., Hou, C., Chen, L., Zhou, D., Ren, K., Zhou, Z., Zhang, R., Liu, X."SETDB1 induces epithelial‑mesenchymal transition in breast carcinoma by directly binding with Snail promoter". Oncology Reports 41, no. 2 (2019): 1284-1292. https://doi.org/10.3892/or.2018.6871
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