Fig. 3: Depletion of G3BP1 impairs canonical SASP signaling through reduction of STAT3 and NF-κB signaling.
From: G3BP1 controls the senescence-associated secretome and its impact on cancer progression
WI-38 cells were treated with siRNA against G3BP1 (siG3BP1 #1 and #2) or scrambled control (siCTL) and assessed during proliferative stage (PRO) and 8-day post-ionizing radiation (+IR). a RNA was extracted and assayed by RT-qPCR using primers against indicated mRNAs. The data are a mean of three independent experiments ± s.e.m (two-tailed unpaired Student’s t test, exact <0.001 p-values from left to right: 0.00095, 0.00022). b Conditioned media from PRO and from +IR WI-38 cells treated with siRNA against G3BP1 (siG3BP1) and scrambled control (siCTL) were analyzed by multiplex arrays. The heatmap indicates the fold change in comparison to the control PRO, SEN siCTL (siCTL), and SEN siG3BP1 (siG3BP1). Relative expression levels per replicate and average fold change differences are shown as indicated in heatmap. c (left) Cell lysates as described were subjected to western blot analysis against indicated proteins. (right) Quantifications represent a mean of relative protein levels from three independent experiments ± s.e.m (two-tailed unpaired Student’s t test, exact <0.001 p-values from left to right: 0.0007). d WI-38 cells as described were analyzed by immunofluorescence with antibody against p65 during PRO and SEN. DAPI staining was used to visualize nuclei. Scale bar, 20 μm. Source Data for panels (a) and (c) are provided in the Source Data File. Raw data for (b) is provided in Supplementary Data 2.
