Fig. 5: HDACi lowers CAF-mediated pro-tumorigenic LIF-STAT3 signaling.
From: Inhibiting stromal Class I HDACs curbs pancreatic cancer progression
a, b RT-qPCR results showing Lif/LIF expression in mCAF (imCAF1, a) and hCAF (YAM, b) cells under Ent treatment (10 μM, 2 d) compared to Veh. c, d Relative abundance of mLIF (c) and hLIF (d) detected by immunoassay in CM from Ent-treated CAFs. e, f Representative images from Western blotting detecting pSTAT3, STAT3 and α-tubulin (TUB, sample processing control) in mouse (p53 2.1.1, e) and human PDAC cells (MIA PaCa2, f) treated with small molecule-depleted CM from Veh- (V) or Ent- (E) treated CAFs, and/or anti-LIF antibody (α-LIF, 4 μg/ml), with quantifications of pSTAT3/STAT3 ratio relative to no CM treatment. g, h Numbers of spheroids formed in p53 2.1.1 (g) and MIA PaCa2 cells (h) with CM, α-LIF antibody (4 μg/ml) and/or recombinant (r) m/hLIF (0.1 μg/ml) treatments. i RT-qPCR results showing the expression of Lif and HDAC genes in imCAF1 cells with shRNAs targeting Hdac1, 2 and 3 (shH1/2/3), compared to shEV. j Relative abundance of mLIF in CM from shH1/2/3 CAFs. k, l Representative images and quantifications of pSTAT3/STAT3 ratio from Western blotting (k) and results from spheroid assay (l) in p53 2.1.1 cells treated with CM from shEV or shH1/2/3 CAFs. RT-qPCR, LIF measurements, Western blotting, n = 3 independent samples; spheroid assays, n = 4 (g, h), 5 (l) cell sample replicates. Data are presented as mean values ± SEM. *p < 0.05; **p < 0.01; ***p < 0.001. Two-sided t-test. Source data including p-values are provided as a Source Data file.
