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Elevated GCN5 expression confers tamoxifen resistance by upregulating AIB1 expression in ER-positive breast cancer

Ji Hoon Oh1, Ji-Yeon Lee1, Kwang H Kim2

  • 1Department of Anatomy, Embryology Laboratory, Yonsei University College of Medicine, Seoul, 03722, South Korea.

Cancer Letters
|September 28, 2020
PubMed

Insights

General control non-derepressible 5 (GCN5) drives tamoxifen resistance in breast cancer by increasing amplified in breast cancer 1 (AIB1) and decreasing p53. Restoring p53 levels can re-sensitize cells to tamoxifen therapy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Estrogen receptor-positive breast cancer constitutes ~70% of cases, often treated with tamoxifen.
  • Tamoxifen resistance develops in approximately one-third of patients, necessitating research into resistance mechanisms.

Purpose of the Study:

  • To investigate the role of general control non-derepressible 5 (GCN5) and its downstream targets in tamoxifen-resistant (TamR) breast cancer.
  • To explore GCN5 as a potential therapeutic target for overcoming tamoxifen resistance.

Main Methods:

  • Analysis of GCN5 levels and proteasomal degradation in TamR-MCF7 cells.
  • Assessment of amplified in breast cancer 1 (AIB1) and p53 expression and stability.
  • In vivo studies to correlate GCN5 and AIB1 with tamoxifen resistance.

Main Results:

  • TamR-MCF7 cells exhibited elevated GCN5 due to reduced proteasomal degradation.
  • GCN5 overexpression led to increased AIB1, decreased p53 stability, and tamoxifen resistance.
  • Forced p53 expression restored tamoxifen sensitivity in GCN5-AIB1-overexpressing cells.
  • In vivo studies confirmed a positive correlation between GCN5, AIB1, and tamoxifen resistance.

Conclusions:

  • GCN5 promotes tamoxifen resistance in breast cancer by upregulating AIB1 and reducing p53 levels.
  • GCN5 and its downstream effectors are potential therapeutic targets to prevent or treat tamoxifen resistance.
Keywords:
Histone acetyltransferaseKAT2ANCOA3p21p53

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