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Article

Loss of breast cancer metastasis suppressor 1 promotes ovarian cancer cell metastasis by increasing chemokine receptor 4 expression

  • Authors:
    • Xiu-Jie Sheng
    • Ying-Qun Zhou
    • Qing-Yuan Song
    • Dong-Mei Zhou
    • Qi-Cai Liu
  • View Affiliations / Copyright

    Affiliations: Department of Obstetrics and Gynecology, The Third Affiliated Hospital of Guangzhou Medical College, Guangzhou 510150, P.R. China
  • Pages: 1011-1018
    |
    Published online on: December 19, 2011
       https://doi.org/10.3892/or.2011.1596
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Abstract

Breast cancer metastasis suppressor 1 (BRMS1) is a predominantly nuclear protein that differentially regulates the expression of multiple genes, leading to suppression of metastasis without affecting orthotopic tumor growth. It has been demonstrated that BRMS1 may be correlated with advanced ovarian cancer. The aim of this study was to investi­gate the mechanisms of BRMS1 involvement in ovarian cancer metastasis. We constructed a plasmid containing a short hairpin RNA (shRNA) against BRMS1 and transfected it into the ovarian cancer cell line OVCAR3. Real‑time reverse transcription polymerase chain reaction (real‑time PCR) and Western blot analyses demonstrated that BRMS1 expression was efficiently downregulated. Stable suppression of BRMS1 significantly enhanced cell adhesion, migration, invasion and angiogenesis. We also found that chemokine receptor 4 (CXCR4) was upregulated at both the mRNA and protein levels. When approaching for the mechanism, we discovered that activation of the nuclear factor‑κB (NF‑κB) signaling pathway mediated CXCR4 upregulation, as demonstrated by the electrophoretic mobility shift assay (EMSA). Collectively, these results suggest that attenuation of BRMS1 may play a critical role in promoting migration, invasion and angiogenesis of ovarian cancer cells and BRMS1 may regulate the metastatic potential at least in part through upregulation of CXCR4 via NF‑κB activation. Restoration of BRMS1 function is thus a potential new strategy for treating human ovarian cancer.
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Copy and paste a formatted citation
Spandidos Publications style
Sheng X, Zhou Y, Song Q, Zhou D and Liu Q: Loss of breast cancer metastasis suppressor 1 promotes ovarian cancer cell metastasis by increasing chemokine receptor 4 expression. Oncol Rep 27: 1011-1018, 2012.
APA
Sheng, X., Zhou, Y., Song, Q., Zhou, D., & Liu, Q. (2012). Loss of breast cancer metastasis suppressor 1 promotes ovarian cancer cell metastasis by increasing chemokine receptor 4 expression. Oncology Reports, 27, 1011-1018. https://doi.org/10.3892/or.2011.1596
MLA
Sheng, X., Zhou, Y., Song, Q., Zhou, D., Liu, Q."Loss of breast cancer metastasis suppressor 1 promotes ovarian cancer cell metastasis by increasing chemokine receptor 4 expression". Oncology Reports 27.4 (2012): 1011-1018.
Chicago
Sheng, X., Zhou, Y., Song, Q., Zhou, D., Liu, Q."Loss of breast cancer metastasis suppressor 1 promotes ovarian cancer cell metastasis by increasing chemokine receptor 4 expression". Oncology Reports 27, no. 4 (2012): 1011-1018. https://doi.org/10.3892/or.2011.1596
Copy and paste a formatted citation
x
Spandidos Publications style
Sheng X, Zhou Y, Song Q, Zhou D and Liu Q: Loss of breast cancer metastasis suppressor 1 promotes ovarian cancer cell metastasis by increasing chemokine receptor 4 expression. Oncol Rep 27: 1011-1018, 2012.
APA
Sheng, X., Zhou, Y., Song, Q., Zhou, D., & Liu, Q. (2012). Loss of breast cancer metastasis suppressor 1 promotes ovarian cancer cell metastasis by increasing chemokine receptor 4 expression. Oncology Reports, 27, 1011-1018. https://doi.org/10.3892/or.2011.1596
MLA
Sheng, X., Zhou, Y., Song, Q., Zhou, D., Liu, Q."Loss of breast cancer metastasis suppressor 1 promotes ovarian cancer cell metastasis by increasing chemokine receptor 4 expression". Oncology Reports 27.4 (2012): 1011-1018.
Chicago
Sheng, X., Zhou, Y., Song, Q., Zhou, D., Liu, Q."Loss of breast cancer metastasis suppressor 1 promotes ovarian cancer cell metastasis by increasing chemokine receptor 4 expression". Oncology Reports 27, no. 4 (2012): 1011-1018. https://doi.org/10.3892/or.2011.1596
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