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Endocrine therapy-resistant breast cancer model cells are inhibited by soybean glyceollin I through Eleanor

Tatsuro Yamamoto1,2,3, Chiyomi Sakamoto1, Hiroaki Tachiwana2

  • 1Department of Medical Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, 2-2-1 Honjo, Chuo-ku, Kumamoto, 860-0811, Japan.

Scientific Reports
|October 14, 2018
PubMed

Insights

Glyceollin I, a soybean polyphenol, inhibits Eleanor non-coding RNAs and estrogen receptor-positive breast cancer cell growth. This offers a new strategy to trigger apoptosis in endocrine therapy-resistant cancer cells.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Endocrinology

Background:

  • Long-term estrogen deprivation (LTED) in estrogen receptor (ER) α-positive breast cancer cells leads to endocrine therapy resistance and estrogen-independent proliferation.
  • A cluster of non-coding RNAs, termed Eleanors (ESR1 locus enhancing and activating non-coding RNAs), form RNA clouds and upregulate the ESR1 gene in LTED cells.
  • Resveratrol inhibits Eleanors via ER, but alternative therapeutic strategies are needed.

Purpose of the Study:

  • To investigate the effect of glyceollin I, a polyphenol from stressed soybeans, on Eleanor RNA clouds and LTED cells.
  • To determine if glyceollin I's inhibitory mechanism involves the estrogen receptor (ER).

Main Methods:

  • Preparation and characterization of glyceollin I from stressed soybeans.
  • Assessment of glyceollin I's effect on Eleanor RNA cloud formation and ESR1 mRNA transcription.
  • Evaluation of glyceollin I's impact on LTED cell proliferation and apoptosis induction.
  • Comparison of glyceollin I's mechanism with resveratrol's ER-dependent inhibition.

Main Results:

  • Glyceollin I was identified as a potent inhibitor of the Eleanor RNA cloud and ESR1 mRNA transcription.
  • Unlike resveratrol, glyceollin I's inhibitory action was independent of the estrogen receptor (ER), suggesting a distinct binding mechanism.
  • Glyceollin I preferentially inhibited the growth of LTED cells and induced apoptosis, highlighting its therapeutic potential.

Conclusions:

  • Glyceollin I exhibits a novel mechanism for inhibiting LTED cells by targeting Eleanor RNAs.
  • This ER-independent pathway offers a new therapeutic avenue for endocrine therapy-resistant breast cancer.
  • Polyphenols like glyceollin I can trigger apoptosis in resistant breast cancer cells through both ER-dependent and ER-independent pathways.

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