Abstract

   Disclosure: B. Flowers: None. A. Zigrossi: None. A. Diamond: None. I.
   Kastrati: None.

   SELENOF is an understudied selenium-containing protein which has
   previously been postulated to behave as a tumor suppressor in the
   breast. Examination of patient databases showed that SELENOF levels
   were lowest in tumors from patients with aggressive late-stage breast
   cancers. Whether loss of SELENOF drives breast tumorigenesis remains to
   be determined. To address this question, we used juvenile female wild
   type or systemic Selenof knockout mice and exposed them to
   7,12-Dimethylbenz[a]anthracene (DMBA), a carcinogen which replicates
   the multistep process of breast tumorigenesis. Previous reports have
   shown that loss of Selenof led to glucose and metabolic dysregulation
   in mice suggesting a link between Selenof and metabolism. Because
   obesity is a risk factor in breast cancer, we challenged the mice with
   a western diet, high in fats and in calories, to mimic obesity. We
   hypothesized that loss of Selenof would promote DMBA-induced
   tumorigenesis and the western diet would exacerbate it. We found that
   tumor incidence was in fact highest in the Selenof knockout mice and
   western diet group. The Selenof knockout mice exhibited higher weights
   and higher fasting glucose levels consistent with metabolic
   dysfunction. These findings indicate that lower or loss of SELENOF
   expression may predispose a subset of women, especially obese ones, to
   increased risk of breast cancer. The link between SELENOF, obesity, and
   breast cancer warrants further investigation.

   Presentation: Thursday, June 15, 2023
     __________________________________________________________________

   Articles from Journal of the Endocrine Society are provided here
   courtesy of The Endocrine Society
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