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. Author manuscript; available in PMC: 2015 Nov 20.
Published in final edited form as: Cell Rep. 2014 Nov 6;9(4):1318–1332. doi: 10.1016/j.celrep.2014.10.011

Figure 5. The STP axis supports the transformed state of breast cancer by restraining REST.

Figure 5

  1. Ectopic SCYL1 and TEX14 reduce endogenous REST protein abundance. BT549 TNBC cells were transduced as indicated and analyzed by western blot.
  2. SCYL1 and TEX14 promote cellular transformation in a REST-dependent manner. Anchorage-independent growth was assessed in the cells from A. Data presented as mean +/− SE.
  3. SCYL1 and TEX14 loss of function increases REST protein abundance. MDA-MB231-LM2 TNBC cells were engineered with the indicated dox-inducible shRNAs. Protein levels were assessed by western blot analysis.
  4. SCYL1 and TEX14 loss of function suppresses cellular transformation. Anchorage-independent growth was assessed in the cells from C +/−dox. Data presented as mean +/− SE.
  5. SCYL1 and TEX14 support the transformed state by restraining REST. MDA-MB231-LM2 TNBC cells engineered with the indicated dox-inducible shRNAs (from C) were transduced with a constitutive control or REST shRNA retrovirus. Protein levels were assessed by western blot.
  6. SCYL1 and TEX14 support the transformed state by restraining REST. Anchorage-independent growth was assessed in the cells from E +/−dox. Data presented as mean +/− SE.