Fig. 3

Cisplatin responsive activation of NF-κB induced PIK3CA in SP fraction of resistant cells. a Schematic of predicted response elements of five transcription factors on full-length PIK3CA promoter identified using JASPER server. b TNFα and LiCl treatment increased OS4-PIK3CA promoter activity only in A2780-CisR but not in A2780. Forskolin induced marginal change in both cells. Fold change (treated/control) were represented in red font (n = 4). c qPCR showed induction in PIK3CA expression only in A2780-CisR but not in A2780 cells after TNFα, LiCl and forskolin treatment. d Both cisplatin and TNFα augmented interaction of NF-κB on PIK3CA promoter as assessed by ChIP assay in A2780-CisR, TOV21G, and SKOV3 cells. e-g Perason correlation analysis showed a strong positive correlation between NF-κB reporter and PIK3CA promoter activity only in SP but not in MP or NSP cells in response to cisplatin. Black -untreated and red -treated. (Note- overlapping values in cisplatin treated MP are appeared as a single dot) (n = 4). h Protein levels of NF-κB pre and post cisplatin treatment. i ChIP assay for NF-κB occupancy on PIK3CA promoter in SP and NSP after TNFα and cisplatin treatment. GAPDH was used as control for ChIP experiments. Data represented as average ± SEM of four independent replicates with their actual p-value for statistical significance (ns-non significant). Also see Additional file 3: Figure S2, Additional file 4: Figure S3 and Additional file 5: Figure S4