Fig 2: Influence of knocking down PELP1 on E2 induced proliferation and invasion of A549 cells. (A) Examining the protein levels of PELP1, ERα, and ERβ by western blot after the A549 cells were transfected with PELP1 siRNA. (B) Examining A549 cell proliferation activity by MTT test. (C) Examining PCNA protein levels by western blot. (D) Examining cell cycle by flow cytometry. (E) Examining cell growing ability formation with colony formation assay. (F) Examining cancer cell migration by wound healing assay. (G) Examining cancer cell invasion by transwell assay. (H) Examining MMP-9 protein levels by western blot. Data were presented from three independent experiments.* compared with control group, p < 0.05; # compared with E2 treated NC group, p < 0.05. WT (wild type), NC (non-specific RNA control).

Fig 3: Combining PELP1 status and Ki-67 LI as a prognostic biological marker. Kaplan–Meier survival curve showed that, combination of PELP1 status with Ki-67 status was significantly correlated with DFS (a1) and OS (a2) in patients with TNBC; patients with TNBC in PELP1/Ki-67 double high group had significantly reduced DFS (b1) and OS (b2) compared with others.

Fig 4: Representative immunohistochemical examples of PELP1 staining. In (A) PELP1 positive low differentiated epithelial ovarian cancer, (B) PELP1 positive high differentiated epithelial ovarian cancer, (C) mucinous ovarian cancer with nearly complete absence of nuclear PELP1 staining and (D) PELP1 negative low differentiated epithelial ovarian cancer is shown. Pictures were taken using TissueFAXS (TissueGnostics; Vienna, Austria; magnification x200).

Fig 5: Immunohistochemical staining of PELP1 in TNBC. Positive immunostaining of PELP1 mainly distributed in nuclei of tumor cells, no cytoplasmic staining was found (a, b). Low grade lymph node stage TNBC showed weak PELP1 nuclear expression (a), High grade lymph node stage TNBC showed strong PELP1 nuclear expression (b). PELP1 nuclear staining was absent in negative control (c). Bar = 50 μm.