| First Author | Gingras S | Year | 2017 |
| Journal | PLoS One | Volume | 12 |
| Issue | 6 | Pages | e0178680 |
| PubMed ID | 28570664 | Mgi Jnum | J:245235 |
| Mgi Id | MGI:5916114 | Doi | 10.1371/journal.pone.0178680 |
| Citation | Gingras S, et al. (2017) SCYL1 does not regulate REST expression and turnover. PLoS One 12(6):e0178680 |
| abstractText | 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. |
