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September 10, 2025Cancer Research

Abstract P36: The Intrinsically Disordered Activation Function 1 of Progesterone Receptor is Required for Regulation of Cell Proliferation

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Authors

PLPheck Khee LauQWQian Yee WooSLShi Hao Lee

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Overview

Observational analysis reveals that mutations in activation function impair cell proliferation in breast cancer cells, suggesting a key regulatory role.

Key Points

  • The KKR/FFF mutation in progesterone receptor significantly impairs progestin-induced cell proliferation in MCF-7 breast cancer cells.
  • RNA-seq analysis shows overall impairment in gene regulation, particularly in cell growth-related genes, due to the KKR/FFF mutation.
  • The study highlights the critical role of the intrinsically disordered activation function in modulating transcription dynamics of the progesterone receptor.
  • Increased interaction between the mutant AF1 and coregulator SRC1 suggests altered transcriptional dynamics without affecting enhancer interactions.

Cite This Study

Lau et al. (2025) studied this question.

synapsesocial.com/papers/68c1a5ff54b1d3bfb60e0246https://doi.org/10.1158/1538-7445.fcs2024-p36
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Ligand-Dependent and -Independent Functions of Activation Function 1 of Progesterone Receptor in Genome-Wide Gene Regulation and in Cell Proliferation and Apoptosis of Breast Cancer Cells2026
  2. 2Abstract 6571: O-GlcNAc sites on progesterone receptor are critical for its ligand independent repression of interferon signaling in breast cancer2024
  3. 3Abstract 3584: Context matters: Genomic profiling of PR isoform-specific actions in breast cancer stem cells reveals novel therapeutic insights for ER+ breast cancer2024
  4. 4Abstract 5364: Progesterone receptor modulates the antigen processing and presentation machinery decreasing MHC class I expression on tumors2024
  5. 5Abstract 2284: Progesterone receptor modulates the antigen processing and presentation machinery: Decreasing MHC class I expression on tumor2026