Transcription factors and hormone receptors: Sex‑specific targets for cancer therapy (Review)

Oncol Lett. 2024 Dec 6;29(2):93. doi: 10.3892/ol.2024.14839. eCollection 2025 Feb.

Abstract

Despite advancements in diagnostic and therapeutic technologies, cancer continues to pose a challenge to disease-free longevity in humans. Numerous factors contribute to the onset and progression of cancer, among which sex differences, as an intrinsic biological condition, warrant further attention. The present review summarizes the roles of hormone receptors estrogen receptor α (ERα), estrogen receptor β (ERβ) and androgen receptor (AR) in seven types of cancer: Breast, prostate, ovarian, lung, gastric, colon and liver cancer. Key cancer-related transcription factors known to be activated through interactions with these hormone receptors have also been discussed. To assess the impact of sex hormone receptors on different cancer types, hormone-related transcription factors were analyzed using the SignaLink 3.0 database. Further analysis focused on six key transcription factors: CCCTC-binding factor, forkhead box A1, retinoic acid receptor α, PBX homeobox 1, GATA binding protein 2 and CDK inhibitor 1A. The present review demonstrates that these transcription factors significantly influence hormone receptor activity across various types of cancer, and elucidates the complex interactions between these transcription factors and hormone receptors, offering new insights into their roles in cancer progression. The findings suggest that targeting these common transcription factors could improve the efficacy of hormone therapy and provide a unified approach to treating various types of cancer. Understanding the dual and context-dependent roles of these transcription factors deepens the current understanding of the molecular mechanisms underlying hormone-driven tumor progression and could lead to more effective targeted therapeutic strategies.

Keywords: androgen receptor; estrogen receptor; hormone; sex-specificity; transcription factor; tumor progression.

Publication types

  • Review

Grants and funding

The present study was supported by the National Research Foundation of Korea (grant nos. 2022R1F1A1076029 and 2022R1A2C1093335).