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. 2020 May 19;11:2487. doi: 10.1038/s41467-020-16051-9

Fig. 6. SH3RF3 enhances PTX3 expression through JNK-JUN pathway.

Fig. 6

a, b PTX3 expression (a) and tumorsphere formation (b, n = 3 culturing experiments) of SH3RF3-overexpressing and control HMLE cells treated with inhibitors of JNK (SP600125, 5 nM), WNT (XAV939, 5 nM), and NF-κB (BAY11-7082, 5 nM). c, d PTX3 expression (c) and tumorsphere formation (d, n = 3 culturing experiments) of SH3RF3-overexpressing and control MDA-MB-231 cells treated with the JNK inhibitor. e JNK and JUN phosphorylation after SH3RF3 overexpression and knockdown. f Expression of JUN-target genes after SH3RF3 overexpression in HMLE (n = 3 qRT-PCR experiments). g ChIP-qPCR analysis of JUN binding to PTX3 promoter in HeLa (n = 3 ChIP experiments). h Luciferase reporter analysis of PTX3 promoter in JUN-overexpressing and control HeLa cells (n = 3 reporter assays). Data represent mean ± SD. Statistical significance was determined by two-tailed unpaired t-test (a, b, d, f, g, and h). The experiments in (a–f) and (g) were repeated three times independently with similar results, and the data of one representative experiment are shown. Source data are provided as a Source data file.