Fig 2: Characterization of ECAD-overexpressing human TSCs and ESCs.a Immunostaining of human TSCs transfected with a CDH1-EGFP expressing plasmid. ECAD expression is triggered upon 1 µg mL-1 DOX addition. b Quantification of GATA3 levels in cells from panel (a). n = 2,052, 589, 285, and 136 cells per condition. Kruskal Wallis test, ****p < 0.0001. Data are shown in a box plot. Whiskers go from minimum to maximum values. The box extends from the 25th to 75th percentile, and the middle line represents the median. c Percentage of phospho-HISTONE H3 (pH3) positive cells in cells from panel (a). n = 2,789, 805, 156, and 183 cells per condition. Chi-square test, *p = 0.018. d RT-PCR analysis of SDC1, HLA-G, and AXIN2 levels in human TSCs that were/were not transfected with a CDH1-EGFP expressing plasmid in the presence or absence of 1 µg mL-1 DOX. Each dot represents one sample. n = 4 samples per condition. One-way ANOVA with a multiple comparisons test, *p < 0.0479, **p = 0.0022. Error bars represent s.e.m. e Immunostaining of human ESCs transfected with a CDH1-EGFP expressing plasmid. ECAD expression is triggered upon DOX addition. f Quantification of NANOG levels in cells from panel (e). n = 2,980, 803, 1,080, and 1,829 cells per condition. Kurskal Wallis test, ns nonsignificant. Data are shown in a box plot. Whiskers go from minimum to maximum values. The box extends from the 25th to 75th percentile, and the middle line represents the median. g Percentage of phospho-HISTONE H3 (pH3) positive cells in cells from panel (e). n = 3,091, 717, 1,497, and 2,243 cells per condition. Chi-square test, ****p < 0.0001. h RT-PCR analysis of NANOG, OCT3/4, and AXIN2 levels in human ESCs that were/were not transfected with a CDH1-EGFP expressing plasmid in the presence or absence of 1 µg mL-1 DOX. Each dot represents one sample. n = 4 samples per condition. One-way ANOVA with a multiple comparisons test, ns nonsignificant. All error bars represent s.e.m. three independent experiments (panels a–c, e–g) and two independent experiments (panels d and h). All scale bars, 50 µm. Source data are provided as a Source Data file.

Fig 3: CXCR4 expression on PCs correlates with the percentage of transferred mitochondria.A Calcein AM labeled HMCLs were cultured alone or with MitoTracker red stained HS-5. Mitochondrial red fluorescence internalization was detected in HMCLs in time-lapse by using operetta. B Quantification of the area under the curve (A.U.C.) ± SD. **** vs U266 and NCI-H929 cell lines. C Flow cytometry analysis of mitochondrial red fluorescence internalized by HMCLs (CD45+ gated) cocultured with MitoTracker red labeled HS-5 cells for 24 h. D Flow cytometry analysis for CXCR4 expression of HMCLs. Representative histograms with the corresponding isotype control (dotted line) are shown. ****vs U266 and NCI-H929 cell lines. CXCR4 expression levels were correlated with the percentage of transferred mitochondria in HMCLs (E) and primary CD138+ cells (F). The data are presented as means ± SD of three independent experiments (**p < 0.01; ***p < 0.001; ****p < 0.0001).

Fig 4: Effects of SDC1 knockdown or overexpression on BC cells’ invasion and migration. (A) Quantitative PCR analysis of SDC1 expression levels in si-SDC1 control, si-SDC1, oe-SDC1 control and oe-SDC1 breast cancer cell lines (MCF-7 and MDA-MB-231). (B) Western blot of SDC1 expression levels in si-SDC1 control, si-SDC1, oe-SDC1 control and oe-SDC1 breast cancer cell lines (MCF-7 and MDA-MB-231). (C) Effects of SDC1 knockdown or overexpressed on invasion of MDA-MB-231 breast cancer cells. (D) Effects of SDC1 knockdown or overexpressed on invasion of MCF-7 breast cancer cells. (E) Effects of SDC1 knockdown or overexpressed on migration of MDA-MB-231 breast cancer cells showed by scratch assays. (F) Effects of SDC1 knockdown or overexpressed on migration of MCF-7 breast cancer cells showed by scratch assays. ***:P < 0.001.

Fig 5: Heatmaps illustrate RNA-Seq differential expression data of the Sdc1, Sdc2, Sdc3, Sdc4, and Sdcbp genes across different prostatic lobes, mouse models, and tumor stages. (A) Non-neoplastic tissue (Pb-Cre4-negative—wild type) controls; (B) Pb-Cre4/Trp53f/f;Rb1f/f double conditional knockout mouse (p53/Rb mouse); (C) Pb-Cre4/Ptenf/f mouse (Pten mouse). The heatmaps represent Log10 of normalized RPKM values. PIN Stage—prostatic intraepithelial neoplasia; MedTumor—medium-stage tumor, micro-invasive adenocarcinomas; AdTumor—tumor in a more advanced stage, invasive adenocarcinomas. Note that significant upregulation of Sdc1 in the Pten mouse (*** p < 0.0001 vs. control group), a significant upregulation of Sdc3, and downregulation of both Sdc2 and Sdc4 in advanced tumors from the p53/Rb mouse were also observed (p < 0.0001 vs. wildtype group).