Fig. 4: SIRT1 partners with DVL1 at ETS1 genomic loci.

a Co-Immunoprecipitation for endogenous DVL1 and ETS1, and probe for endogenous DVL1, ETS1 and SIRT1 in the cytoplasmic and nuclear fraction. Representative blots shown (three biological replicates); IgG heavy chain was the loading control for IP. b ChIP and ChIP/re-ChIP/re-ChIP (n  =  3 biological replicates (3 technical replicates each), mean ± SD, two-way, ANOVA, followed by Dunnett’s multiple comparison test was used to test significance) for HA-DVL1, ETS1, and SIRT1 in the same genomic region in MDA-MB-231 and HEK293TREx cells. c RT-qPCR identifies significant (n  =  3 biological replicates (3 technical replicates each), mean ± SD, two-way, ANOVA followed by Sidak’s multiple comparison test was used to test significance) alteration of gene expression with SIRT1 IV inhibitor in MDA-MB-231 and HEK293TREx cell lines. d ChIP-qPCR (n  =  3 biological replicates (3 technical replicates each), mean ± SD, two-way, ANOVA, followed by Sidak’s multiple comparison test was used to test significance) of HA-DVL1, ETS1, and SIRT1 in ETS1-regulated genes in both cell lines. e Illustration demonstrating SIRT1 partners with DVL1, and DVL1 partners with both ETS1, SIRT1, and other possible co-factors (CoF) at the same genomic loci in the promoter to regulate gene expression, top; inhibition of SIRT1 in MDA-MB-231 prevents binding of DVL1 and ETS1 to genomic loci, and alters gene expression, bottom right; inhibition of SIRT1 in HEK293TREx changes DVL1 and ETS1 binding potential, altering gene expression. Created in BioRender. Martinez, D. (2025) https://BioRender.com/ebwkjhc. Source data are provided as the Source Data file.