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Targeting the ELF1/EGFR/ERK positive feedback loop overcomes resistance to androgen receptor inhibition in AR-Vs positive prostate cancer
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DOI：10.1016/j.neo.2026.101324.png)
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Abstract
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• Long-term enzalutamide exposure of AR-Vs positive PC cells triggers an AR-independent bypass through the transcriptional upregulation of EGFR. • Identification of an ELF1/EGFR/ERK positive feedback loop that sustains oncogenic signaling and drives enzalutamide resistance. • Pharmacological inhibition of EGFR using gefitinib restores enzalutamide (or mithramycin) sensitivity in resistant CRPC cells and patient-derived organoids. • Elevated EGFR protein expression correlates with high Gleason scores and serves as a robust predictor of shorter PFI and DFI in prostate cancer patients.
Keywords:
Prostate cancer
AR-Vs
Enzalutamide resistance
ELF1/EGFR/ERK
Therapeutic vulnerability
AR inhibition
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