Endonuclease FEN1 coregulates ERα activity and provides a novel drug interface in tamoxifen resistant breast cancer.
By: Koen D Flach, Manikandan Periyasamy, Ajit Jadhav, Dorjbal Dorjsuren, Joseph C Siefert, Theresa E Hickey, Mark Opdam, Hetal Patel, Sander Canisius, David M Wilson, Maria Donaldson Collier, Stefan Prekovic, Marja Nieuwland, Roelof Jc Kluin, Alexey V Zakharov, Jelle Wesseling, Lodewyk F A Wessels, Sabine C Linn, Wayne D Tilley, Anton Simeonov, Simak Ali, Wilbert Zwart

Molecular Oncogenomics, The Netherlands Cancer Institute.
2020-03-09; doi: 10.1158/0008-5472.CAN-19-2207
Abstract

Estrogen receptor α (ERα) is a key transcriptional regulator in the majority of breast cancers. ERα-positive patients are frequently treated with tamoxifen, but resistance is common. In this study, we refined a previously identified 111-gene outcome prediction-classifier, revealing FEN1 as the strongest determining factor in ERα-positive patient prognostication. FEN1 levels were predictive of outcome in tamoxifen-treated patients, and FEN1played a causal role in ERα-driven cell growth. FEN1 impacted the transcriptional-activity of ERα by facilitating coactivator recruitment to the ERα transcriptional complex. FEN1 blockade induced proteasome-mediated degradation of activated ERα, resulting in loss of ERα-driven gene expression and eradicated tumor cell proliferation. Finally, a high-throughput 465,195 compound screen identified a novel FEN1 inhibitor, which effectively blocked ERα-function and inhibited proliferation of tamoxifen-resistant cell lines as well as ex-vivo cultured ERα-positive breast tumors. Collectively, these results provide therapeutic proof-of-principle for FEN1 blockade in tamoxifen-resistant breast cancer.



Copyright ©2020, American Association for Cancer Research.

PMID:32193286






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