Fig. 3

Knockdown of CEBPD suppresses VAMP3 transcription and cell autophagy. A intersections of top 1,000 candidate CEBPD targets with DEGs screened from GSE28784 and GSE90564 datasets; B correlations between CEBPD and HEY1 and OS of breast cancer analyzed by Kaplan–Meier Plotter analysis; C expression of VAMP3 in biopsy tissues of SD/PD (n = 18) and CR/PR (n = 23) patients measured by IHC assay. Parental or PTX-resistant TNBC cells were administered lentivirus-carried sh-CEBPD or sh-NC. D mRNA and protein levels of VAMP3 in cells detected by qPCR and WB analysis (n = 3); E autophagy activity in cells analyzed by immunofluorescence staining of LC3 (n = 3); F putative binding relationship and binding sites between CEBPD and VAMP3 promoter; G binding of CEBPD with VAMP3 promoter validated by ChIP-qPCR assay (n = 3); H regulatory role of CEBPD in VAMP3 transcription in 293 T cells with sh-NC or sh-CEBPD transfection determined by luciferase assay (H) (n = 3). Differences were analyzed by the t-test (C), one-way ANOVA followed by Tukey's multiple comparisons test (D-E) or by the two-way ANOVA followed by Sidak's post-hoc test (G-H). *p < 0.05