Fig. 1

PAD2 expression is highly upregulated in tamoxifen-resistant breast cancer, and depletion of PAD2 facilitates the sensitivity of MCF7/TamR cells to tamoxifen. a Analysis of PAD2 mRNA levels in clinical tumor tissue microarray during tamoxifen therapy using the publicly GEO dataset GDS806/11785. b Endogenous PAD2 mRNA levels in tamoxifen-resistant breast cancer cell line MCF7 (MCF7/TamR) were compared to tamoxifen-sensitive controls (MCF7/TamS). GAPDH served as controls. c, d Endogenous PAD1–4 mRNA and protein levels in MCF7/TamR cells were determined by qRT-PCR (c) and Western Blot (d). GAPDH served as loading control. e Stable PAD2 knockdown efficiency was confirmed by qRT-PCR and immunoblot. GAPDH served as loading control. f MCF7/TamR cell proliferation was not affected upon PAD2 depletion by CCK8 assay, compared to the empty vector (shCon) control cells. g Cell proliferation was inhibited in PAD2 knockdown MCF7/TamR cells by CCK8 assay, in the presence of 7 μM tamoxifen, compared to the empty vector (shCon) control cells. h 7 μM tamoxifen treatment on TamR/MCF7 cells showed a time-dependent inhibition of cell proliferation. *P < 0.05. i The mice bearing PAD2 knockdown cells exhibited smaller tumors than the mice with shRNA control cells post tamoxifen treatment (n = 3/group). The volume of tumors at indicated time after cell implantation was quantified, and the average volume was plotted. *P < 0.05