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SOX9/FXYD3/Src Axis Is Critical for ER

Yue Xue1, Lihua Lai1, Wenwen Lian1

  • 1Institute of Immunology, Zhejiang University School of Medicine, Hangzhou, China.

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|September 13, 2018
PubMed
Summary
This summary is machine-generated.

A newly identified SOX9/FXYD3/Src pathway is crucial for maintaining estrogen receptor-positive breast cancer stem cells and tamoxifen resistance. Targeting FXYD3 may offer a new therapeutic strategy for hormone therapy-refractory breast cancer.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Cancer stem cells (CSCs) drive poor prognosis and drug resistance in breast cancer.
  • Molecular mechanisms maintaining CSC function, particularly in estrogen receptor-positive (ER+) breast cancer, are not fully understood.

Purpose of the Study:

  • To elucidate the molecular regulatory network governing ER+ breast CSC function.
  • To identify novel therapeutic targets for endocrine therapy-resistant ER+ breast cancer.

Main Methods:

  • Analysis of FXYD3 expression in ER+ breast CSCs.
  • Investigation of the regulatory relationship between SOX9 and FXYD3.
  • Examination of FXYD3 interactions with Src and ERα.
  • Assessment of the role of the SOX9/FXYD3/Src axis in CSC maintenance and tamoxifen resistance.

Main Results:

  • FXYD3, an estrogen-inducible gene, is upregulated in ER+ breast CSCs and crucial for their function.
  • FXYD3 amplification mediates tamoxifen resistance in ER+ breast cancer cells.
  • SOX9 directly promotes FXYD3 expression, and FXYD3 is essential for SOX9 nuclear localization, forming a positive feedback loop.
  • FXYD3 interacts with Src and ERα to activate Src-mediated non-genomic estrogen signaling, supporting ER+ CSCs.

Conclusions:

  • The SOX9/FXYD3/Src axis plays a critical role in maintaining ER+ breast CSCs and endocrine resistance.
  • Targeting the FXYD3-mediated pathway presents a potential therapeutic strategy for hormone therapy-refractory ER+ breast cancer.