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ITE, an endogenous aryl hydrocarbon receptor ligand, suppresses endometrial cancer cell proliferation and migration

Yiding Bian1, Yiran Li2, Garima Shrestha1

  • 1Clinical and Translational Research Center, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai, PR China.

Toxicology
|April 7, 2019
PubMed
Abstract

Insights

The aryl hydrocarbon receptor (AhR) ligand, ITE, suppressed endometrial cancer (EC) cell proliferation and migration. This study supports ITE as a potential therapeutic for EC treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Endometrial cancer (EC) requires novel therapeutic targets, particularly for therapy-resistant cases.
  • The aryl hydrocarbon receptor (AhR), a transcription factor, exhibits tumor-suppressive properties.
  • Investigating endogenous AhR ligands like ITE offers a potential treatment strategy.

Purpose of the Study:

  • To determine if the endogenous AhR ligand, ITE, influences EC cell proliferation and migration via AhR.
  • To evaluate AhR expression in EC tissues compared to normal tissues.

Main Methods:

  • Quantitative real-time PCR and Western blot analyzed AhR expression in EC and normal tissues.
  • Transwell assays assessed ITE's impact on EC cell proliferation and migration in vitro.
  • Mouse xenograft models evaluated ITE's in vivo efficacy.

Main Results:

  • AhR expression was mildly elevated in EC tissues versus adjacent normal tissues.
  • ITE treatment inhibited EC cell proliferation and migration in vitro.
  • ITE suppressed tumor growth in mouse xenograft models.

Conclusions:

  • ITE demonstrates significant anticancer effects against endometrial cancer cells in vitro and in vivo.
  • ITE represents a promising small molecule therapeutic candidate for endometrial cancer treatment.
Keywords:
2-(1′H-indole-3′-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE)Aryl hydrocarbon receptor (AhR)Endometrial cancerMigrationProliferation

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