Gingras Sebastien, Kuliyev Emin, Pelletier Stéphane
Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States of America.
Embryonic Stem Cell Laboratory, Department of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee, United States of America.
PLoS One. 2017 Jun 1;12(6):e0178680. doi: 10.1371/journal.pone.0178680. eCollection 2017.
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.
最近的一项研究将SCYL1鉴定为致癌性STP轴的组成部分之一，该轴通过调节REST肿瘤抑制因子的降解来促进三阴性乳腺癌。与该研究结果相反，在此我们通过使用3种不同的基因方法表明，SCYL1并不调节REST的周转。具体而言，Scyl1+/+和Scyl1-/-小鼠胚胎成纤维细胞中的REST蛋白水平和周转情况相同。同样，使用CRIPSR-Cas9技术在Hek293T细胞中靶向失活SCYL1并不影响REST的稳态水平和周转。此外，RNA干扰介导的Hek293T或MDA-MB-231细胞中SCYL1的缺失并未改变REST的稳态水平和周转。总之，我们的研究结果表明，SCYL1对REST的周转没有作用，因此不支持先前一项表明SCYL1在介导REST降解中起作用的研究。
