Epigenetic suppression of FBXL7 promotes metastasis

Loredana Moro; Michele Pagano

doi:10.1080/23723556.2020.1833698

Epigenetic suppression of FBXL7 promotes metastasis

Mol Cell Oncol. 2020 Oct 22;7(6):1833698. doi: 10.1080/23723556.2020.1833698.

Authors

Loredana Moro^{1

2

3}, Michele Pagano^{1

2

4}

Affiliations

¹ Department of Biochemistry and Molecular Pharmacology, New York University Grossman School of Medicine, New York, NY, USA.
² Perlmutter NYU Cancer Center, New York University Grossman School of Medicine, New York, NY, USA.
³ Institute of Biomembranes, Bioenergetics and Molecular Biotechnologies, National Research Council, Bari, Italy.
⁴ Howard Hughes Medical Institute, New York University Grossman School of Medicine, New York, NY, USA.

Abstract

Epigenetic reprogramming is emerging as a key mechanism for metastasis development. Our study identified a novel regulatory mechanism whereby promoter methylation-mediated epigenetic silencing of the gene encoding the ubiquitin ligase subunit F-box/LRR-repeat protein 7 (FBXL7) induces accumulation of active c-SRC, which, in turn, activates epithelial-to-mesenchymal transition and supports cancer cell invasion and metastasis.

Keywords: Epigenetics; c-SRC; epithelial-to-mesenchymal transition; metastasis; ubiquitin ligase.

Abstract

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