MassIVE MSV000095057

Partial Public PXD053178

Title: Site specific O-GlcNAcylation of progesterone receptor (PR) supports PR attenuation of interferon stimulated genes (ISGs) and tumor growth in breast cancer

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Description

Hormone receptor (HR) positive breast cancer, defined by expression of estrogen (ER) and/or progesterone (PR) receptor expression, is the most commonly diagnosed type of breast cancer. PR alters the transcriptional landscape to support tumor growth in concert with or independent of ER. Understanding the mechanisms regulating PR function are critical to developing new strategies to treat HR+ breast cancer. O-GlcNAc is a post-translational modification responsible for nutrient sensing that fine tunes protein function. We have previously reported O-GlcNAcylation on PR. Although PR is heavily post translationally modified, primarily through phosphorylation, specific sites of O-GlcNAcylation on PR, and how they regulate PR action, have not been investigated. Using established PR-expressing breast cancer cell lines, we mapped the sites of O-GlcNAcylation on PR. RNA-sequencing revealed site-specific O-GlcNAcylation of PR is critical for ligand-independent suppression of interferon signaling, a regulatory function of PR previously studied in our lab. Furthermore, O-GlcNAcylation of PR enhances PR-driven tumor growth in vivo. We have delineated one mechanism regulating PR function in breast cancer that impacts tumor growth, and provided additional insight into the mechanism through which PR attenuates interferon signaling. [doi:10.25345/C5V11VX5V] [dataset license: CC0 1.0 Universal (CC0 1.0)]

Keywords: Breeast canter, proteomics, OGlcNAc

Contact

Principal Investigators:
(in alphabetical order) 		Chad Slawson, University of Kansas Medical Center, USA
Chrity Hagan, University of Kansas Medical Center, USA
Submitting User: aartigues
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