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. Author manuscript; available in PMC: 2017 Nov 20.
Published in final edited form as: Nat Genet. 2017 Jan 16;49(3):367–376. doi: 10.1038/ng.3753

Figure 5. PGD-dependence in distant metastatic subclones.

Figure 5

(a) Western blots against indicated histone modifications performed on peritoneal (A38Per) and distant metastatic (A38Lg) subclones from the same patient showed that global levels of reprogrammed H3K9me2 and acetylation in A38Lg were reversed by removal of glucose from the media (left panel), PGD RNAi (middle panel), and 6AN treatments (right panel). (b) Western blots on A38Lg indicated that PGD knockdown by RNAi did not perturb expression of other PPP components or KRAS. (c) PGD RNAi did not affect the ability of HPDE cells or regional PDAC samples to form tumors in 3D matrigel assays (representative photomicrographs shown with quantified numbers of tumors/well, n=4 technical replicates, error bars: s.d.m.). (d) In contrast, PGD RNAi significantly reduced tumor formation across distant metastatic subclones (n=4 technical replicates, error bars: s.d.m., *p<0.01 by two tailed t-tests). Scale bars: 400μm.