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. 2022 Apr 19;13(4):374. doi: 10.1038/s41419-022-04826-5

Fig. 5. p65 is targeted by NOB to inhibit TNBC.

Fig. 5

A Diagram indicating the p65-inducible system. B MDA-MB-231 cells were grown to confluence and treated NOB with (20 µM) and tetracycline (100 nM) for 12 h. WST-1 assays were performed at 72 h after NOB treatment. Mock indicates pCW 57.1 vector (Empty template vector). Data represent mean ± SEM. Two-way ANOVA with Sidak’s multiple comparisons test, **p < 0.01, and ***p < 0.001. C Wound-healing assay. The closure of wounds in MDA-MB-231 cells after 16 h of p65 induction by tetracycline (100 nM). The results are presented as relative motility to the width at 0 h (100%). Data represent mean ± SEM. Two-way ANOVA with Sidak’s multiple comparisons test, *p < 0.05 and ***p < 0.001. D Colony formation assays were performed with 20 µM NOB. Data represent mean ± SEM. Two-way ANOVA with Sidak’s multiple comparisons test. **p < 0.01 and ***p < 0.001. E–I RNA-seq analysis. E Volcano plot of 4937 differential expressed genes (DEGs) between DMSO and NOB treatment MDA-MB-231 cells (p < 0.05 and fold change >2). Plots highlighted with red and green represent up- and downregulated genes. Multiple NF-κB pathway genes are marked. F Pie chart of protein-coding genes, LncRNA, and other genes in the DEG set. G Gene ontology analysis of DEGs with DAVID. Top-ranked pathways are presented, including NF-κB signaling indicated with red. H KEGG analysis of DEGs with ClusterProfiler. Top-ranked pathways are presented, including “Pathway in cancer ”. I Gene set enrichment analysis demonstrated the enrichment of gene sets related to cancer.