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Fig. 6 | Journal of Experimental & Clinical Cancer Research

Fig. 6

From: Inhibiting NR5A2 targets stemness in pancreatic cancer by disrupting SOX2/MYC signaling and restoring chemosensitivity

Fig. 6

NR5A2 promotes stemness by diminishing MYC expression. A qPCR analysis for NR5A2, MYC and PPARGC1A mRNA levels following 72 h of treatment with Cpd3 (40 µM). B Change in oxygen consumption rate (OCR) indicative of mitochondrial respiration following 72 h of treatment with Cpd3 (40 µM) for adherent cultures (Adh, differentiated cancer cells) or sphere cultures (Sph, enriched for CSCs). C Change in extracellular acidification rate (ECAR) indicative of glycolysis following 72 h of treatment with Cpd3 (40 µM) in Adh or Sph cultures. D Change in OCR following overexpression (OE) of NR5A2 in differentiated cancer cells. E Percent input of immuno-precipitated DNA at the MYC promoter following treatment with Cpd3 (40 µM). The intergenic region is used as a negative ChIP control. F OCR levels for shNT or shMYC, following 72 h treatment with DMSO (Ctrl) or Cpd3 (40 µM). G qPCR of mRNA levels for NR5A2, SOX2 and MYC in shNT or shMYC cells, following 72 h of treatment with DMSO (–) or Cpd3 (40 µM). H Changes in maximal (max.) respiration and ATP production in shNT or shMYC cells, following 72 h treatment with DMSO Ctrl (–) or Cpd3 (40 µM). In panels A, E, G, and H data are presented as mean ± SD and statistically analyzed using two-tailed Mann–Whitney tests to compare two groups (n = 4 biological replicates). The asterisk * indicates significance for p < 0.05. Please also see Supplementary Fig. 5

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