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. 2022 May 31;298(7):102082. doi: 10.1016/j.jbc.2022.102082

Figure 4.

Figure 4

FOXF2 activates the Wnt signaling pathway in luminal breast cancer cells but inhibits that in BLBC cells by directly targeting WNT2B and FZD1.A, the indicated cells were cotransfected with TOP/FOP flash and Renilla pRL-TK plasmids for 48 h and then subjected to a dual-luciferase reporter assay to detect Wnt signaling pathway activity. The ratio of TOPflash to FOPflash was analyzed. B, nuclear translocation of β-catenin in the indicated cells was analyzed by immunoblot. WC: whole-cell extracts; Cy: cytoplasmic extracts; Nu: nuclear extracts. C, the binding of FOXF2 to the WNT2B and FZD1 promoters containing the putative binding sites in the indicated cells transfected with FOXF2-FLAG plasmids was assessed by ChIP-qPCR assays. D, the transcriptional activity of the WNT2B and FZD1 promoters in the indicated cells was evaluated by a dual-luciferase reporter assay. pGL3-WNT2B or pGL3-FZD1 promoter luciferase reporter construct containing or lacking the FOXF2-binding element was transfected into the indicated cells. E and F, the mRNA (E) and protein (F) levels of WNT2B and FZD1 in the indicated cells were detected by RT-qPCR and immunoblot. ∗, p < 0.05 compared with control cells. BLBC, basal-like breast cancers; ChIP-qPCR, chromatin immunoprecipitation-quantitative PCR; RT-qPCR, reverse transcription-quantitative PCR.