Submit

Login Login

Register Register

Home / Journals / OR / Online First / doi:10.32604/or.2026.071328
Journal Menu
Special Issues
Table of Content

All issues

Online First

2026

2025

2024

2023

2022

2021

2020

2019

2018

2017

2016

2015

Past Issues

Open Access

ARTICLE

Inhibitory Effect of Progesterone on Breast Cancer Progression and Migration via the Regulation of Epithelial-Mesenchymal Transition

So-Ye Jeon1,#, Zeeshan Ahmad Bhutta1,#, Hong Kyu Lee2, Kyung-Chul Choi1,*
1 Laboratory of Biochemistry and Immunology, College of Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk, Republic of Korea
2 Department of Companion Animal Health, College of Biomedical Science & Health, Inje University, Gimhae, Republic of Korea
* Corresponding Author: Kyung-Chul Choi. Email: email
# These authors contributed equally to this work
(This article belongs to the Special Issue: Breast Cancer Biomarkers and Drug Targets Discoveries Towards a More Personalized Treatment Setting)

Oncology Research https://doi.org/10.32604/or.2026.071328

Received 05 August 2025; Accepted 26 December 2025; Published online 30 January 2026

Abstract

Objectives: Progesterone (P4) is believed to inhibit breast cancer growth, but its role in counteracting estrogen (E2)-driven progression remains unclear. This study aimed to investigate the inhibitory effect of P4 on E2-induced cell proliferation, migration, and invasion in Estrogen receptor (ER)+/progesterone receptor (PR)+ breast cancer cells by examining its regulatory role in the epithelial-mesenchymal transition (EMT). Methods: ER and PR-positive MCF-7 clonal variant (MCF-7 CV) breast cancer cells were treated with E2 and co-treated with various concentrations of P4. The effects on cell proliferation, migration, and invasion were assessed. The expression of key EMT markers (E-cadherin, N-cadherin, vimentin), transcription factors (Snail, Slug), and apoptosis-related genes (p53, B-cell lymphoma 2 [BCL-2], BCL2-associated X [BAX]) were analyzed. Results: P4 significantly inhibited E2-induced cell proliferation in a dose-dependent manner. In the presence of E2, P4 treatment reversed EMT characteristics by increasing E-cadherin while decreasing N-cadherin, vimentin, Snail, and Slug. Consequently, P4 inhibited E2-stimulated cell migration and invasion. Furthermore, P4 treatment promoted apoptosis by upregulating BAX and p53 and downregulating BCL-2. Conclusion: Progesterone can counteract estrogen-driven breast cancer progression in ER+/PR+ cells by inhibiting proliferation, reversing the EMT process, and inducing apoptosis. These findings provide mechanistic insight into the protective role of PR signaling in breast cancer.

Keywords

Progesterone; breast cancer; epithelial-mesenchymal transition

  • 96

    View

  • 15

    Download

  • 0

    Like

Related articles
Copyright© 2026 Tech Science Press
© 1997-2026 TSP (Henderson, USA) unless otherwise stated

Share Link