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Breast Cancer Research and Treatment

, Volume 133, Issue 1, pp 145–159 | Cite as

Alteration of Y-box binding protein-1 expression modifies the response to endocrine therapy in estrogen receptor-positive breast cancer

  • Tokiko Ito
  • Shinobu Kamijo
  • Hiroto Izumi
  • Kimitoshi Kohno
  • Jun Amano
  • Ken-ichi ItoEmail author
Preclinical Study

Abstract

Y-box binding protein-1 (YB-1) plays an important role in tumor progression and drug resistance. This study examined whether YB-1 is involved in the alteration of response to endocrine therapy in estrogen receptor (ER)-positive breast cancer cells. MCF7 cells that stably expressed YB-1 (MCF7-YB-1) and vector control cells (MCF7-vector) were established. These cells were used to analyze the expression of the factors related to ER and growth factor receptor signaling pathways and responses to antiestrogens (tamoxifen and fulvestrant) and estrogen responsive element (ERE) activity. The effect of knocking down endogenous YB-1 expression was tested in wild-type MCF7 cells. In addition, the expression of YB-1 and the factors related to ER and growth factor receptor signaling pathways were evaluated in clinical breast cancers treated with preoperative chemotherapy. The expression of HER2, AIB1, p-Erk, and c-Myc was increased in MCF7-YB-1 cells. In contrast, knocking down of YB-1 decreased the expression of these factors but increased the expression of ERα in wild-type MCF7 cells. Furthermore, sensitivity to antiestrogens was decreased in the MCF7-YB-1 in comparison to that in MCF7-vector cells. The introduction of YB-1 into MCF7 cells inhibited apoptosis and cell cycle arrest at G1 phase induced by antiestrogens. In MCF7-YB-1 cells, the expression levels of p-Erk and c-Myc were continuously upregulated when cells were treated with either tamoxifen or fulvestrant. The ERE activity was reduced in MCF7-YB-1 cells in comparison to MCF7-vector cells, and the ERE activity in MCF7-YB-1 cells was inhibited by fulvestrant at a lower concentration than that which inhibited the ERE activity in MCF7-vector cells. In ER-positive clinical breast cancers treated with preoperative chemotherapy, significantly more number of specimens that showed increased or positive YB-1 expression after chemotherapy was positive for HER2 expression. These data suggest that alteration of YB-1 may modify the crosstalk between the ER pathway and HER2 pathway in ER-positive breast cancer cells, and consequently, may alter the response to endocrine therapy in ER-positive breast cancer cells.

Keywords

YB-1 Breast cancer Endocrine therapy Crosstalk 

Notes

Acknowledgment

We would like to thank Dr. Shin-ichi Hayashi for providing the ERE promoter construct.

Conflicts of interest

The authors declare that they have no competing interests.

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Copyright information

© Springer Science+Business Media, LLC. 2011

Authors and Affiliations

  • Tokiko Ito
    • 1
  • Shinobu Kamijo
    • 2
  • Hiroto Izumi
    • 3
  • Kimitoshi Kohno
    • 3
  • Jun Amano
    • 2
  • Ken-ichi Ito
    • 1
    Email author
  1. 1.Division of Breast and Endocrine Surgery, Department of SurgeryShinshu University School of MedicineMatsumotoJapan
  2. 2.Department of SurgeryShinshu University School of MedicineMatsumotoJapan
  3. 3.Department of Molecular BiologyUniversity of Occupational & Environmental HealthKitakyushuJapan

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