Exploring the putative role of EGFR in prostate cancer: Interactions with androgen and estrogen receptors
EGFR interacts with androgen and estrogen receptors in prostate cancer, influencing tumor progression and suggesting that simultaneous targeting of EGFR and hormone receptor pathways may improve treatment of castration‑resistant disease
The epidermal growth factor receptor (EGFR) is a transmembrane tyrosine kinase receptor that plays a critical role in regulating cell proliferation, survival, and differentiation. Aberrant activation or overexpression of EGFR has been observed in several cancers, including prostate cancer (PCa), and is associated with aggressive tumor behavior and poor prognosis. The development and progression of PCa largely depend on the involvement of androgen receptor (AR) pathways, which are directly related to EGFR signaling. Research indicates that EGFR can affect AR activity, increasing transcriptional activity or promoting ligand‑independent activation, which may lead to castration‑resistant prostate cancer (CRPC). Furthermore, emerging evidence suggests that estrogen receptors (ERs) may also interact with EGFR signaling in prostate tissue. These may influence tumor growth, interactions with cellular plasticity, and therapy resistance, but their exact mechanisms require further investigation. Identifying and improving treatment strategies for advanced and treatment‑resistant PCa requires understanding the interplay between the EGFR, AR, and ER pathways. However, clinical trials have shown limited success in targeting EGFR alone, possibly through compensatory mechanisms via steroid hormone receptors. Therefore, therapies that simultaneously target EGFR and AR/ER activity may be more effective. Continued research into the molecular interplay between these pathways will broaden our understanding of prostate cancer biology and support the development of more personalized and effective treatments.
Understanding the EGFR‑aromatase and EGFR‑ER interaction in prostate cancer can reveal new therapeutic combinations to overcome resistance and improve outcomes for patients with advanced or castration‑resistant disease.
Evidence level: Korai humán adat. Kis vagy feltáró emberi adat.
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