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. 2015 Sep 23;6:8257. doi: 10.1038/ncomms9257

Figure 1. BTG2 expression is regulated by SETD1A.

Figure 1

(a) Knockdown of SETD1A specifically induces BTG2. A lentiviral shRNA screen against H3K4 KMTs in MDA-MB-231 cells shows that SETD1A depletion specifically induces BTG2 expression compared with pLKO-infected control cells. Fold change in BTG2 and KMT expression after 72 h of viral infection is shown with controls set at 1. The dotted line marks twofold induction of BTG2 compared with control. KMTs and BTG2 are shown as red and blue/green bars, respectively. (b) Total proteins isolated from control and SETD1A-depleted MDA-MB-231 cells were analysed for H3K4Me1, H3K4Me2, H3K4Me3, total histone H3 and ß-actin protein expression. (c) SETD1A suppresses BTG2 in prostate and lung cancer cells. SETD1A and BTG2 expression in SETD1A-depleted cells represents the average derived from cells individually infected with the two different shSETD1A constructs (shSETD1A#1 and shSETD1A#2), with the shGFP-infected control set at 1. (d) Expression of lentivirally expressed SETD1A in MCF10A cells decreases BTG2 expression (white bar). Fold expression of SETD1A in control and SETD1A-infected cells is shown (black bar). (e) WDR82, a non-catalytic subunit of the SET1/COMPASS complex, regulates BTG2 expression. WDR82 and BTG2 expression in WDR82-depleted MDA-MB-231 cells represents the average derived from cells individually transfected with the two different siWDR82 sequences, with the siNT (non-targeting, NT)-transfected control set at 1. Data are represented as mean±s.d. of the average of three experimental replicates. Asterisks indicate P values of P<0.05 for a,c–e by Student's t-test.