scyl1 does not regulate rest expression and turnover.

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ID: 147660
2017
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Abstract
A recent study identified SCYL1 as one of the components of the oncogenic STP axis, which promotes triple-negative breast cancer by regulating degradation of the REST tumor suppressor. Contrary to the findings of that study, herein we show by using 3 distinct genetic approaches that SCYL1 does not regulate REST turnover. Specifically, REST protein levels and turnover were identical in Scyl1+/+ and Scyl1-/- mouse embryonic fibroblasts. Similarly, targeted inactivation of SCYL1 in Hek293T cells by using CRIPSR-Cas9 technology did not affect REST steady-state level and turnover. Furthermore, RNA interference-mediated depletion of SCYL1 in Hek293T or MDA-MB-231 cells did not alter REST steady-state level and turnover. Together, our findings indicate that SCYL1 does not contribute to REST turnover and thus do not support a previous study suggesting a role for SCYL1 in mediating REST degradation.
Reference Key
gingras2017plosscyl1 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Sebastien Gingras;Emin Kuliyev;Stéphane Pelletier
Journal ensaio pesquisa em educação em ciências
Year 2017
DOI
10.1371/journal.pone.0178680
URL
https://doi.org/10.1371/journal.pone.0178680
Keywords
medicinescience

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